Michael Worobey’s Wobbly Research into the Early History of HIV

Michael Worobey’s wobbly research into the early history of HIV.

In late October and early November 2007 there was coverage in several media outlets (mainly in the US) of a newly-published study entitled “The Emergence of HIV/AIDS in the Americas and Beyond”. The lead author was Michael Worobey, an assistant professor of ecology and evolutionary biology at the University of Arizona in Tucson.

Worobey’s study focuses on the early spread of HIV-1 and AIDS out of Africa – and to the rest of the world. It concludes that, after it emerged from Africa, the first staging-post of pandemic HIV-1 was on the island of Haiti, and that it was from there that the virus later moved on to the United States and Canada. (The phrase “pandemic HIV-1” is used to mean the type of HIV that is found predominantly in North America and Europe: the so-called “Euro-American strain” of HIV-1, known officially as HIV-1 Group M, sub-type B.)

In itself this seems a reasonable hypothesis, one that was first mentioned in the non-medical literature as long ago as 1987, when it was proposed in Randy Shilts’ seminal book on the AIDS epidemic, “And The Band Played On” [New York: St Martin’s Press]. It is one of several hypotheses that seek to explain how the human immunodeficiency virus arrived on the North American continent, three of which are outlined below.

Hypothesis 1. The Africa – Haiti – North America transmission hypothesis favoured by Worobey is also supported by historical data, for it is known that thousands of Haitian teachers and technocrats worked in the Democratic Republic of Congo (the DRC, the former Belgian Congo) in the 1960s, after the exodus of Belgian officials in and after 1960, the year of Independence, left a critical vacuum. . (The DRC is now almost universally accepted as representing the initial hearth of pandemic AIDS.) Haitians were ideal replacements for the Belgians, being well-educated, French-speaking, black – and more than eager to leave a country dominated by the dictatorships of the Duvaliers.

Hypothesis 2. This hypothesis proposes that subtype B might have travelled straight from Africa to North America where it infected a gay or bisexual man who later infected a Haitian counterpart (probably a bisexual, and very possibly during a vacation). Again, there is some historical support, for during the 1970s gay cruises from the US were extremely popular, and almost all featured Haiti as one of the most favoured stopovers.

Hypothesis 3. In The River, I wrote about another possibility: that the virus was exported first from Africa to Europe (and in particular to West Germany), and thence to Haiti and the US. In support of this, the first two retrospectively diagnosed AIDS cases in West Germany date from 1976 and 1977, and thus predate the earliest recorded gay cases from the Americas; both were male patients who died in January 1979 (one of whom is known to have been an active gay/bisexual). A third significant early case was a gay German chef who died of AIDS in Manhattan in 1980, after spending the three previous years working in Haiti, where he first displayed symptoms. This man apparently originated from Gelsenkirchen, the same city where Zaire (as the DRC was called from the 1970s to the 1990s) played two of its three games in the 1974 World Cup; thousands of Zairois came to Germany to support their team. Where, one wonders, was this man infected – in Haiti or Germany?

Hypothesis 4.

There is also a fourth possible hypothesis about how HIV-1 might have arrived in North America and Haiti, one that was tentatively advanced in my book “The River” in 1999. The clue that prompted this hypothesis was an apparently anachronistic historical detail. The earliest convincing case of AIDS in the United States involved a female baby born in New Jersey in 1973 or 1974 to a sixteen-year-old girl, who was identified as a drug-injector who had had multiple male sex partners. The infant died in 1979 after having shown the symptoms of AIDS for 5 years; her stored tissues later tested positive for HIV-1. Because the baby’s case of AIDS predates any other known AIDS case in North America by at least four years, it would seem to have real significance.

The strong indications are that she was infected perinatally by her teenage mother, who must have been born at some point between 1956 and 1958. Might it be, I wondered, that 16 years earlier, the mother had been one of the infants born to women prisoners at Clinton State Farms in Clinton, New Jersey in the ten years beginning 1955, nearly all of whom were experimentally vaccinated with Hilary Koprowski’s oral polio vaccines?

From late 1955 onwards, Koprowski and his team used Clinton Farms as a convenient North American testing-ground for their early OPVs, and it is therefore eminently possible that they tested not only batches of vaccine that had been produced in the US, but also vaccine batches that had been prepared locally in the Belgian Congo.

Former Koprowski aide Stanley Plotkin has reported that this Clinton hypothesis has been disproved, but I can demonstrate that his claim is incorrect.

There is considerably more to report on this subject, but I feel that this is not the right time to place these matters in the public domain.

[However, more detailed information about the early history of HIV-1 and AIDS in North America, Haiti, and West Germany may be found in chapters 3 to 5 of The River (pages 55 to 88), and more about the Clinton hypothesis appears on pages 692-700 and 778-779.]

The inherent bias of Worobey’s paper.

In his Americas paper [PNAS; 2007; 104 (47); 18566-18570; official e-pub October 31st, 2007; formal publication November 20th, 2007], Dr Worobey states that his analysis of the sequences of 122 persons infected with HIV-1 Group M subtype B indicates a 99.8% probability that Hypothesis 1 is correct, and that the subtype B virus travelled from Africa to Haiti to North America, and not by any other route.

On the face of it, the conclusions of Worobey’s paper seem reasonable enough. But there is a huge caveat about this work.

The 122 subtype B sequences on which the work is based consist of five sequences from early Haitian AIDS patients tested in the USA, and 117 subtype B sequences selected from the HIV/AIDS Sequence Database, (after attempts were made to exclude atypical strains and strains which suggested that they might be recombinant in origin). The five early Haitian sequences all apparently came from a Florida doctor, Arthur Pitchenik, who had gathered samples from Haitian men who had emigrated to the US in or after 1975, and whose blood was taken in either 1982 or 1983, after they had first displayed symptoms of AIDS. (It would seem, therefore, that some of these men may have been living in the US for 7 or 8 years before they fell sick.)

As additional historical background (not considered by Worobey), the first plausible case of AIDS from Haiti itself was a retrospectively identified case from 1978, and 7 further plausible Haitian cases have been identified from the years 1978 and 1979. Four of these eight cases from the 1970s were from Haiti itself, and four involved Haitians living in Canada and the US.

Save for the intriguing paediatric AIDS case from New Jersey mentioned above, the first American to show symptoms of AIDS did so in the first quarter of 1978. A total of 12 US cases (11 in gays/bisexuals) were retrospectively identified from 1978 and 1979 (one of whom may have been Haitian; [Selik RM, “Acquired Immune Deficiency Syndrome (AIDS) Trends in the United States, 1978-1982”; Am. J. Med.; 1984; 76; 493-500.] (However, in other papers the first Haitian with AIDS in the US is documented as presenting in early 1980.)

By the end of 1981 there were hundreds of American AIDS cases, and Haitians were one of four risk groups who were indiscreetly described by certain CDC scientists as “The 4 Hs”: homosexuals, heroin injectors, haemophiliacs and Haitians.

Of course, this historical background begs a question. Where are the viral sequences from the early AIDS cases from the US – the cases that did not involve Haitian immigrants?

The earliest US HIV-1 sequences included in Worobey’s study are eight sequences dating from 1981 and one from 1982. Although the eight 1981 sequences predate the earliest Haitian sequences in the study by one year, this may not be very significant. This is because, as far as I can determine, all nine of these early US sequences are from gay/bisexual men, and the epidemiological evidence suggests that HIV-1 only entered the hothouse atmosphere of the gay bath-houses in 1977-8, after which the virus spread like wildfire. (The fact that the first people in the world to be identified with AIDS were gay American men was probably a function of the fact that multiple partner exchange, especially in the bath-houses, allowed a large number of gay men to become infected with HIV very rapidly. Partly because of the weight of numbers, and partly because multi-partner gay sex also encourages a wide range of other infections, it was almost inevitable that some of these gay men became “fast progressors”, and progressed rapidly to showing symptoms of AIDS. We now know that roughly 1% of HIV-infected persons display frank symptoms of AIDS in less than a year.)

It is therefore apparent that many of the US AIDS cases who provide the 1981 and 1982 sequences in Worobey’s study may only have been infected with HIV since 1978-1980. By contrast, the five Haitian AIDS patients tested in 1982-3 may not have been fast progressors, and may well have been HIV-infected before leaving Haiti as early as 1975. (It is worth noting that 1975 represented the peak year for “boat people” – Haitians who escaped to the US by sea.)

In short, Worobey finds that the five Haitian sequences are more ancient (set deeper in the phylogenetic tree) than the US sequences, but this may merely, or mainly, be a function of the fact that the Haitian patients were infected in an earlier year, as in all likelihood they were. So what he may actually be recording here is the year of initial infection.

To guard against this possibility, he surely needs to include in the study some sequences from US citizens who were infected back in the 1970s.

And indeed, there is no obvious reason why earlier US HIV-positive serum samples were not also studied. Huge numbers of serum samples were taken from gay and bisexual American men for many different studies throughout the 1970s. In particular, starting in 1977-8, sera were routinely gathered from hundreds of gay and bisexual men in five different North American cities (including New York, Los Angeles and San Francisco), as part of the Five Cities Study. The earliest retrospectively proven HIV-positive serum sample comes from a gay man tested in New York on September 6th, 1977 – but within the next 27 months a viral explosion took place, for both the San Francisco and New York cohorts referred to above were retrospectively found to have levels of HIV-positivity of above 10% by the end of 1979!

Yet as far as I know, there has never been any molecular analysis of HIV-1 viruses from these 1970s sera, or from the stored tissues or sera of US AIDS cases from the 1970s.

What, I wonder, would be the result if the US sequences included in Worobey’s study had included sequences obtained from the very beginning of the gay epidemic, or from one or more of the seven HIV-positive babies (all born to drug-injecting mothers in New York and San Francisco, many of whom may also have been prostitutes) in 1977? [See River, pages 71-72.] Or what if his study had included a viral sequence from the HIV-infected baby born to a drug-injecting New Jersey mother in 1973-4 (alluded to in Hypothesis 4 above)?

I believe that if sequences from early US AIDS patients (or, indeed, early German AIDS patients) had also been included in this study, the outcome of the molecular analysis might have been different.

For instance, such a study might conclude that HIV-1 travelled first from Africa to the Americas, and was then exported via a US infectee to Haiti, where it first entered the gay/bisexual community, and was then re-exported back into the US and Canada a few years later, perhaps via a gay cruiser, or else one of the boat people, thousands of whom fled Haiti for Florida from 1975 onwards. Or else such a study might conclude that the virus had actually travelled from Africa to Germany to Haiti to the US.

In short, it may well be that the findings of Worobey’s study were almost inevitable, given his choice of samples. Under these circumstances, I would propose that his conclusions (that HIV-1 arrived in Haiti before it came to the US) cannot be relied upon. When a study is biased in its selection of samples, it is hard to draw any meaningful conclusions.

The strange dearth of early molecular data from the US.

The lack of any molecular studies of early HIV-positive stored sera and tissues from the United States is remarkable, and deserves further comment.

It would seem that North American doctors are keen to do molecular analysis on potential AIDS cases and HIV infectees from Africa (many studies); the UK (the famous case, apparently later refuted, from 1959: the so-called “Manchester sailor”) and the Caribbean (Worobey’s research), yet there is apparently a total lack of studies of early US and Canadian HIV-infected sera and tissues, and thus no molecular analysis of early North American HIV sequences.

This great gap in the published research also extends to epidemiological studies of the US epidemic. Beginning in 1990, I conducted interviews with doctors from the CDC and elsewhere who were involved in the early days of the American AIDS epidemic. In retrospect, one thing I repeatedly noticed was that nobody from the CDC was willing to talk about the earliest cases.

People such as Jim Curran, the epidemiologist who was the first head of AIDS research at the CDC, and who was the last author of the aforementioned “AIDS trends in the US, 1978-82” paper, were notably reticent about these crucial cases. I was asking for details such as dates, places and symptoms, and not for the names of patients, so there was no need for excessive confidentiality. Despite this, I met with a wall of silence. The only witnesses who were more forthcoming on this topic were a couple of doctors who had left the CDC, and with their cautious help (allied to information obtained from Shilts’s epic book, “And The Band Played On”), I managed to reconstruct a fair part of the early US epidemic (see Chapter 3 of The River).

Many questionable decisions were made in those days. For instance, Shilts relates that the notebooks of the epidemiologist who had single-handedly tracked the early spread of AIDS in San Francisco were shredded by the local public health department within two months of her retirement, with patient confidentiality apparently cited as the reason. These days, such wilful destruction of vital epidemiological data would appear breathtakingly irresponsible.

For studies of ancient sera and tissues, the names of patients or serum donors are automatically withheld, which removes the risk of compromising patient confidentiality. This makes it truly remarkable that no virological studies of early US samples, and no molecular analyses of early US HIV-1 viruses, have yet been carried out (or at least reported in the medical literature).

Is it possible that these vital ancient samples have been autoclaved (just as that early epidemiological data from California was apparently shredded)? I very much doubt it. But in that case, why the dearth of early HIV-1 studies from the US itself? Is it possible that there are concerns that such analyses might reveal some inconvenient or embarrassing information?

The unique prehistory of Subtype B.

There is one further strange historical detail that needs to be mentioned. From the late 1970s onwards, HIV-1 Group M Subtype B experienced epidemic spread in North America and Europe (and indeed in the rest of the world outside Africa). In fact, in many parts of the world outside Africa, it quickly became the dominant strain of HIV.

And yet in Africa itself subtype B apparently either never existed, or else quickly died out. Indeed, until the last few years, the only strains of HIV-1 subtype B ever detected in Africa came from three or four blood samples obtained in the 1990s, which in all likelihood represented viruses that had been re-imported to Africa from the West.

The only plausible candidate for a genuine African subtype B virus was one that was retrospectively reported in 2001. It came from a serum sample from a Congolese woman from Kinshasa who was originally tested at some point between 1983 and 1985. Some 15 years later, her virus was among a group of HIV-1 viruses from the DRC that was sequenced by Tom Folks’ retrovirology team from the CDC with the results published as: M.L. Kalish, T.M. Folks et al., “Evidence for the Presence of all Known HIV-1 Group M Subtypes and Some Unclassifiable Strains in Kinshasa, Zaire, in the Early to Mid-1980s”; 8th Conference on Retroviruses and Opportunistic Infections; 2001; Abstract 268.

Every single one of the major subtypes of pandemic HIV-1 (ten, in those days) had been found in this early sampling of the city of Kinshasa – a unique and hugely significant result.

The presence of a subtype B virus in that city was especially fascinating. In 2002 I e-mailed Folks, asking whether he thought that this 1983-5 subtype B had been a local virus (ie one originating from Zaire, now called the DRC) or a Western re-import, and he e-mailed back: “Only a hunch, but I would guess home (local) infection.”

I found this implausible, in that it was his own team that had sequenced the virus, and yet we then heard nothing more about it – as we surely would have done, if this had been the only genuine sample of African HIV-1 subtype B in existence.

Five years later I asked Folks (now retired from the CDC) the same question, and on December 16th, 2007 he e-mailed back a different answer: “Yes, I agree, it would be strange to find it [the subtype B sequence] there [in Kinshasa] if it were not reimported, but of course, no proof.”

It appears, therefore, that (alone of all the subtypes) the molecular biologists have found no genuine examples in Africa of HIV-1 subtype B.

Of course, the ancestor of all subtype B viruses could still have existed in the DRC back in the 60s, and could have caused onward spread to Haiti, the US and the rest of the world, before dying out in the DRC itself.

Alternatively, the OPV theory (and in particular the Clinton sub-hypothesis outlined above) clearly provide another possible explanation.

This sub-hypothesis would beggar the following questions:

  1. What if the original subtype B virus existed in a vaccine batch that was prepared in the Belgian Congo in the 1950s, but was either never given to humans in that country, or else used only on a limited scale in the Congo, causing only sporadic infections that were insufficient to spark a full-scale subtype B outbreak in that continent?
  2. And what is this same batch was among those sent back to the US for laboratory testing, and was also tested in vivo on an infant or infants from the women’s prison in Clinton, New Jersey?

Depending on one’s beliefs about origins, this scenario may or may not seem far-fetched. But I believe that it is no more far-fetched than the scenario proposed by Michael Worobey, which is based on a whole series of assumptions, none of which are scientifically proven.

When one examines the information (including historical details) available from a number of different sources, rather than making a theoretical analysis that is solely based on a phylogenetic dating theory that has been shown to be inherently flawed, it is revealed that Worobey’s near-certainties are actually based on rather flimsy ground.

Hypothesis 1 (the Africa-to-Haiti hypothesis favoured by Worobey) is a perfectly plausible hypothesis, and may indeed reflect what actually happened historically. However, I firmly believe there is nothing in Worobey’s paper that disproves Hypotheses 2, 3 or 4.

Worobey’s wobbly dating analysis.

In a press release dated October 29th, 2007, Professor Worobey also proposed some dates to flesh out his transmission scenario. He suggested that HIV-1 arrived in Haiti from Africa in “about 1966”, and that the first American was infected with a Haitian version of the virus in “about 1969”. This was sexy stuff, and it engendered coverage in several newspapers.

The latter date is somewhat earlier than many previous estimates, such as those which placed the arrival of HIV-1 in the United States in the early to middle 1970s, mainly on the basis of epidemiological analysis. It requires HIV-1 to have been circulating in the US for 12 years before AIDS was first recognised and reported (in Los Angeles in 1981). I find this rather implausible, but it is certainly not impossible.

What is far less plausible, and in fact highly controversial, is the use of phylogenetic or molecular analysis to try to date the age of HIV-1 isolates.

A brief aside. The early molecular analysis of immunodeficiency viruses by people such as Beatrice Hahn, Paul Sharp and Bette Korber was incredibly useful. It illustrated, for instance, that a simian immunodeficiency virus (SIV) discovered in a Tanzanian baboon had been acquired from a local African green monkey (perhaps one that the baboon had attacked or eaten); this was one of the earliest proofs that cross-species transmission of SIVs occurred in the wild.

And the systematic surveys of SIVs in primates that these and other doctors are currently conducting in different parts of Africa (which have recently discovered an SIV in the gorilla, one that is related to – and probably derived from – chimpanzee SIV) continues to this day to provide dramatic and important new information.

But unfortunately, as the activities of these researchers have grown and their grants have multiplied, some of them have over-reached themselves and have started to make exaggerated or misplaced claims.

Their attempts to date the events on their family tree of SIVs and HIVs is perhaps the best example of science that is based on assertion, rather than on solid scientific principles.

I strongly believe that their research into the “molecular dating of HIV” is inherently unscientific, because it is based on a false premise. This premise is that HIV-1 mutates at a constant rate, according to a molecular clock that beats like a metronome – and that this mutation rate can be measured and used to calculate the dates of significant events in the virus’s early history.

Or to put it in Worobey’s own words, from an interview he did with National Public Radio on November 12th, 2007: “Because viruses mutate at a relatively constant rate, you can actually calibrate what we call a molecular clock, and when we did that we find [sic] that the US epidemic basically – all of it – traces back to what looks like a single migration event of the virus, somewhere around 1969, plus or minus a couple of years.”

In reality, this molecular clock approach is a reasonable approach for dating DNA-based viruses like smallpox, which evolve almost exclusively through mutation. However, it begins to fail for RNA-based viruses, and in particular retroviruses, where a substantial degree of evolution occurs through recombination. Recombination occurs when two different viruses meet inside a cell, and exchange portions of each other’s genomes (much as a male and female human have sex and produce a baby with the genetic characteristics of both parents).

Recombination is a totally different form of evolution from mutation, and it cannot be measured by a molecular clock.

HIV-1 is the most recombinogenic human virus (ie the human virus most prone to recombination) known to medical science. A study published back in July 2002 spelt out just how recombinogenic this virus is. In its title it referred to “massive recombination” and it revealed that recombination is four to ten times more common than mutation in both HIV and SIV. [S. Wain-Hobson et al., “Network analysis of human and simian immunodeficiency virus sequence sets reveals massive recombination resulting in shorter pathways”; J. Gen Virol.; 2002; 84; 885-895.] This important paper also revealed the direct implication of this finding: that HIV sequences were in reality younger (ie closer to the present) than had been anticipated by molecular dating analysis.

A commendably fair-minded commentary on this “really interesting and beautiful study” written by Science staff writer and AIDS specialist Jon Cohen (himself no friend to the OPV theory in the past) concluded that it “raises significant questions about phylogeny trees that attempt to date the origin of HIV, all of which intentionally discard suspected recombinants to make the data interpretable”. [Science; 2002; 297; 312-313.]

As Wain-Hobson and Cohen highlight, all that geneticists such as Michael Worobey can do in their dating attempts is to exclude obvious recombinant HIV-1 sequences from their analyses, so that what they are left with are sequences that have supposedly evolved only through mutation.

In reality, however, HIV-1 sequences that recombined early in their evolutionary history can no longer be identified or recognised, and therefore cannot be excluded from the geneticists’ analyses. In short, there is no way of knowing whether or not any given HIV-1 sequence features ancient recombination.

What this means in practice is that evolutionary dating analysis of HIV-1 is inherently flawed, and that it tends to promote dates of origin that are (a) unreliable, and (b) too far back in the past.

Perhaps the best-known example of HIV-1 phylogenetic dating was published in 2000 by Professor Bette Korber’s team at the HIV Sequence Database at Los Alamos. This was a paper published in Science, which proposed that the Most Recent Common Ancestor (MRCA) of pandemic HIV-1 existed in about 1931 (plus or minus 10 or 15 years). [Korber B. et al.; “Timing the ancestor of the HIV-1 pandemic strains”; Science; 2000; 288; 1789-1796.] Effectively, Korber was proposing a date of origin for the HIV-1 virus in Africa, and thus a start date for the global AIDS pandemic.

The publication of the paper was promoted by a huge press conference, and it naturally garnered world-wide headlines. The science it proposed was elegantly presented, but it was essentially fantasy.

It is noteworthy that Michael Worobey stresses that his dates for the arrival of HIV-1 in Haiti and the US are broadly consistent with this 1931 start date.

In reality, the principal HIV-1 molecular daters turn out to be quite a small group of American, British and Belgian scientists who tend in practice to come up with dates that are consistent with Korber’s ancestral date of 1931. This in turn may mean one of two things:

  1. That the work of all these scientists from Korber onwards is remarkably accurate, even though they are using a molecular clock to try to measure the mutation rate of a virus that evolves mainly through recombination, or
  2. That the findings in Korber’s original study were dubious, and that all HIV-1 molecular dating studies since then have been equally dubious, as they have strived for internal consistency with Korber. In short, that these researchers’ results tend automatically to be self-confirming.

I personally favour scenario (b), and I am not alone. Many scientists with whom I have spoken and corresponded, including molecular biologists and population geneticists, believe that in reality, the molecular dating studies of HIV-1 represent a 21st century version of alchemy, the medieval science which claimed that base metals could be “transmuted” into gold. In the Middle Ages, alchemy was an accepted science. Nowadays, alchemy is viewed with gentle amusement, since it is recognised that the basic premises and assumptions underlying that “science” were wrong.

With the molecular dating of HIV-1 so many different parameters are possible, most notably the selection or rejection of different HIV-1 sequences and the choice of the specific model used to create the molecular clock, that one can arrive at any one of a rather wide variety of dates in the final results column. It therefore becomes relatively easy to come up with dates of origin that tie in with one’s preconceptions, and to convince oneself that one is producing great science when all one is actually doing is reflecting and repeating dubious science of the past.

The latest type of model that the HIV-1 molecular daters (including Worobey in his “Americas” study) like to use is called a “relaxed molecular clock”, which allows the mutation rate to vary among the various HIV-1 sequences. In lay terms this means a clock that does not always act like a clock. With such a clock, it is not so difficult to bend time.

However, a recent key paper from this school of phylogenetic daters (Anne-Mieke Vandamme’s group from the University of Leuven, a seat of learning which was a major collaborator on Koprowski’s 1950s CHAT vaccination trials in Africa) contains rather revealing information about the limitations of these procedures. It concedes how difficult it is, even among the major HIV-1 subtypes, to identify recombinant sequences, and states the following: “As current phylogenetic methods are not capable of accurately reconstructing the evolutionary histories of highly recombinant strains, it may never be possible to correctly assign for all strains which one is the recombinant and which one is the parent.” [Abecasis AB, Vandamme AM et al.; “Recombination confounds the early history of human immunodeficiency virus type 1; subtype G is a circulating recombinant form”; J. Virol.; 2007; 81 (16); 8543-8551.]

(Finally, it is worth pointing out that Vandamme’s group at Leuven is not unique, for nearly all the American, British and Belgian phylogenetic daters mentioned above are either from labs which collaborated directly with Koprowski in the CHAT trials in Africa in the 1950s, or else are scientists who are known to have had contacts in the recent past either with Koprowski’s former deputy Stanley Plotkin, or Plotkin’s group of anti-OPV collaborators. Whether this is significant or coincidental in not yet apparent.)

Possible explanations for the phylogenetic dating mumbo-jumbo.

Outside the heady atmosphere of the molecular dating labs, an increasing number of scientists have over the last seven or eight years realised that molecular dating analyses for HIV-1 are unreliable. The fact that relatively few have spoken up about it is mainly a factor of the way Science is conducted today.

The origins-of-AIDS controversy is one of the most politically-loaded debates in Science. Over the years many scientists (some of whom are generally regarded as eminent) have spoken to me off-the-record, on the basis that I never mention their names. There is widespread concern that getting involved in this debate on the “wrong” side could turn out to be injurious to your health (ie to your funding and career prospects).

This fear may seem incredible, or exaggerated. If you think so, then cast your mind back to the 1930s, when millions of Germans (and indeed, Britons and Americans and others) found it acceptable, or possible, to cast a blind eye to what the Third Reich was doing in Germany. Let me be absolutely clear: I am not suggesting that the HIV-1 geneticists are Nazis! I am merely underlining that there are many ways in which (and levels on which) beliefs, whether or not they are sincerely held, can be transformed into dogma. I am also stressing the fairly obvious fact that because the man and woman in the street (and indeed, the scientist in the lab) don’t have the time to investigate every scientific issue for themselves, they tend in practice to accept much of what they are told by scientists who have spent years studying those particular issues, and who are perceived as experts. In reality, it is not that easy to question the expertise of “experts”.

The dissenting scientists referred to above all expressed deep-seated scepticism about the molecular dating of HIV-1, but insisted that I treat their words as either unattributable or off-the-record. Of course, I have respected their wishes. However, there are also some highly experienced scientists who have spoken up on the record. I am keeping some up my sleeve for now, but two who have come out publicly are professors Gerry Myers and Mikkel Schierup.

In 2000, Professor Myers had recently retired from his job as head of Group T-10 at the Los Alamos National Laboratory (the group responsible for compiling the HIV Sequence Database), where he had been Bette Korber’s boss. Despite having health problems at the time, Myers wrote an intelligent and powerful critique of Korber’s HIV-1 dating work. Gerry Myers was not well enough to fly to London to present this paper at the Royal Society conference on “Origins of HIV and the AIDS epidemic”, but it was presented instead by a young statistician who had co-authored the paper, Tom Burr. [T. Burr, G. Hyman and G. Myers, “The origin of AIDS: Darwinian or Lamarckian?”; Phil. Trans. Roy. Soc. (London) B; 2001; 356; 877-888].

However, five months earlier I had flown to Los Alamos to meet with Myers (for the second time) in order to discuss the molecular analysis of HIV-1. A classicist by training, Myers is a logical and independent thinker, and during our April 2000 meeting he gave me a clear sense of the extent of the disagreement and uncertainty that had existed among the HIV phylogeneticists about how best to undertake the dating of ancient HIV-1 isolates.

In his Royal Society paper, Professor Myers found Professor Korber’s dating approach inherently flawed and questioned some of the specifics of her work. However, as he has told me and others on several occasions, he feels constrained from presenting a more sustained critique, partly because Korber is a personal friend of himself and his family.

Another open critic was the Danish population geneticist Mikkel Schierup, whose paper entitled “Recombination and Phylogenetic Analysis of HIV-1” was first presented at the 2001 meeting on HIV origins at the Lincei Academy in Rome; [Atti dei Convegni Lincei; 2003; 187; 231-245]. Schierup’s paper ably dismantled the molecular dating approach for HIV-1 by using deliciously understated scientific language. Sadly, the closing speaker at that conference (Robin Weiss) together with Paul Sharp (who also spoke at the conference, but who later withdrew his paper from the published proceedings) and his fellow HIV daters have found it easiest to ignore the import of Schierup’s paper.

So why is misleading research based on the molecular dating of HIV-1 promoted and published in the pages of the major scientific journals? The answer may be fairly simple. It ties in with the vague but non-controversial bushmeat hypothesis of origin of AIDS, which proposes that the AIDS pandemic arose through Africans eating or butchering chimpanzees in or around the 1930s. Moreover, it appears to refute the Oral Polio Vaccine (OPV) hypothesis of origin, which proposes that AIDS arose through the experimental vaccination of some 900,000 Africans in the Belgian Congo (now the DRC), and what is now Rwanda and Burundi, with vaccine grown in chimpanzee cells in the late 1950s.

Unfortunately, Michael Worobey now appears to be a committed molecular dater, just like his mentors, molecular biologists Bette Korber and Paul Sharp. As a result, he tends to come out with sweeping and unreliable statements. For instance, in his November 12th, 2007 interview on NPR, he said the following: “[T]here’s a lot of evidence that [the HIV-1] virus was circulating in central Africa for many, many years before it emerged elsewhere in the world.” Worobey went on: “That evidence comes in part from” the fact that similar viruses are found in African apes and monkeys, and that these primates are sold as bushmeat in African markets.

That was all the explanation he gave. In reality, this constitutes no evidence at all, merely a hypothesised mode of transmission which has never been supported by a single compelling piece of evidence.

I believe that Worobey’s claim (that HIV-1 had been circulating for “many, many years before it emerged elsewhere in the world”) is unreliable. Even if one accepts Korber’s date of 1931 plus or minus 10 or 15 years for the emergence of HIV-1 in Africa (which, remember, is an entirely theoretical calculation), this would place emergence in Africa only some 25-35 years before Worobey’s date of export to the rest of the world. This is hardly “many, many years before”, especially when one considers that Africans must have been killing, skinning and eating SIV-infected primates for hundreds of thousands of years!

Given the premises and vague assumptions of the bushmeat school, I would have expected HIV-1 to have emerged in Africa not in 1931, but in 1931 BC….or perhaps 1931000 BC!

The question that the molecular daters prefer not to ask.

I often wonder how these HIV phylogenetic daters can avoid asking themselves what seems to me to be the key question. The question is this. Why is it that, according to them, ten separate transfers of SIV from African primates to man have all occurred during the recent past (in fact, during the middle part of the twentieth century), whereas Africans have been eating and butchering chimps and other monkeys since time immemorial?

According to their own analysis, these ten primate-to-human transfers comprise seven transfers of sooty mangabey SIV to make HIV-2 Types A to G (only two of which, Types A and B, have spread further among humans to cause actual human outbreaks), and three transfers to humans of chimpanzee SIV to make HIV-1 Group M (causing pandemic AIDS), Group N and Group O.

I believe that these geneticists are actually caught in a cleft stick. On the one hand, they cannot argue that HIV and AIDS existed as far back as the early 19th century, because it is easy to prove that those millions of Africans who were forcibly taken to the Americas during the Slave Trade were not infected with any of the HIVs. So this is where their much-vaunted phylogenetic dating analysis comes in. This allows them to argue that those ten proposed transfers of SIVs to Homo sapiens occurred during the 20th century, but only during the first half of the twentieth century, a few vital years before the polio vaccination campaigns of the 1950s and 1960s!

The molecular biologists contend that the index case of the AIDS pandemic, the very first HIV-1, existed in 1931. So why, according to them, was no AIDS seen in Africa before the 1960s or 1970s? They argue that it must have been there, but went unrecognised (a) because the numbers infected were smaller, and (b) because these early cases were instead diagnosed as one of the typical AIDS indicator diseases, such as tuberculosis.

To my mind (and here I am confident of the support of many Africa-based clinicians), this rather jesuitical argument actually demonstrates a basic misunderstanding, or misinterpretation, of the clinical presentation of African AIDS. In reality, AIDS very rarely presents as just a single disease such as TB. In reality it usually presents with a striking range of opportunistic infections (such as oral thrush, and certain specific – and untreatable – dermatological, respiratory and enteropathic complaints) which allows it to be recognised surprisingly quickly. (In the years before AIDS was identified, such a case would have been recognised as striking and unusual; from the 1980s onwards it would have been recognised as AIDS.)

Indeed, this is a key point about AIDS, one that I tried to make in the opening chapters of The River. Even to inexperienced observers, the condition of AIDS is readily recognised as something that is different and new. For instance, the first cases in the Rakai district of southern Uganda were seen in 1982, and by 1984 the local people had given this apparently new disease a new name: “Slim”. (This was even before Slim was recognised by Western doctors in Africa as a presentation of AIDS.) The Sharps and Worobeys, by contrast, apparently believe that thousands of Africans must have been infected between the 1930s and the 1960s, but that nobody noticed that anything new was going on!

In any case, even if one were to accept their 1931 start date as accurate, there is another possible explanation, one that is I believe far more compelling. As I have reported since year 2000, experimental polio vaccination campaigns that used vaccines grown in the kidneys of (a) chimpanzees; and (b) baboons and “other monkeys” (including sooty mangabeys) were staged in Africa in the 1950s and early 1960s, in the very places which are now known and accepted as the geographical hearths of HIV-1 and HIV-2.

The geneticists assume that the various outbreaks of AIDS all evolved from a single index case of HIV infection. However, their molecular dating approach cannot distinguish between one single HIV infection in, say, 1931, and a small cluster of index cases infected via the African vaccines used in the late 1950s. This is because, according to their model, their 1931 index virus would, over 25 or 30 years, have evolved genetically to the same extent that would obtain if multiple HIV-1 variants were introduced to humans in the late 1950s via different batches of vaccine.

To put it another way, the geneticists believe that the nine or so genetically divergent subtypes of HIV-1 group M (pandemic HIV-1) all evolved from that one index case between the 1930s and the 1950s, whereas I believe that the different HIV-1 subtypes represent the different viral strains that were transferred to humans via the different vaccine batches. (It appears that the OPV batches given to humans in Africa were produced in series, one from another, so there is the potential for new chimp viruses to have entered the “soup” and recombined every time that new chimp tissue cultures and chimp sera were employed to grow a new batch of vaccine.)

In short, despite the two very different scenarios for first transfer proposed by the bushmeat and OPV hypotheses, the epidemiological (and phylogenetic) patterns from the late 1950s onwards would be exactly the same.

Has there been a cover-up?

Major scientific journals such as Science, Nature, and the Proceedings of the National Academy of Sciences continue to publish the impressive-sounding (but ill-supported) scientific research of researchers such as Bette Korber and Michael Worobey, while refusing all submissions that contain material or analysis supportive of the OPV hypothesis, even submissions from men as eminent as Bill Hamilton.

Why are these leading scientific journals showing such apparent bias? I believe that the reasons are partly financial and political, and partly ideological.

The Belgian Congo vaccination campaign was master-minded by American and Belgian scientists, and they and their successors can be imagined to be far from happy at the prospect of being sued for billions by large numbers of AIDS patients, for instance in a class action suit.

The governments of the USA and Belgium, both of which backed the trials financially and administratively, may feel very much the same way, and be every bit as defensive.

As for the ideological reasons, vaccination is the Holy Grail of Modern Medicine, and is the process on which most public health interventions are based. It is therefore also the process that can never be allowed to be seriously questioned or criticised in the public domain.

Never mind that I repeatedly emphasise in my writings that most vaccination campaigns are safe, and that I am simply questioning the safety of one experimental campaign conducted in the 1950s. From the perspective of many (far too many) of those in the public health fraternity, it’s a case of never mind what happened in the past: OPV/AIDS is a “dangerous theory” that could adversely affect popular confidence in the vaccination campaigns of the future.

I believe that the bias, as evidenced in part by the censored coverage in major scientific journals, is so extensive that it amounts to an implicit cover-up. Unfortunately, many scientists do not have the time or inclination to investigate these matters themselves, and they therefore tend to accept what Nature and Science have already pronounced on the subject. In practice, this means accepting the assurances of well-known scientists such as British retrovirologist Robin Weiss, who is, I believe, one of the principal architects and promulgators of the “official” bushmeat version of how AIDS began.

In response to my book The River in 1999, Professor Weiss wrote a cautious, but basically positive, review in Science, and then helped organise the Royal Society meeting on “Origins of HIV and the AIDS Epidemic” in September 2000. He skilfully arranged and co-ordinated that meeting so that it highlighted the establishment response to the OPV hypothesis, a response that was based on (a) the bushmeat hypothesis, (b) phylogenetic dating analysis, and (c) the testing of samples of CHAT vaccines obtained in the US and UK.

The latter samples of vaccine had never themselves been used for vaccination in Africa, and they clearly represented different batches of vaccine from those used in Africa (although Weiss and others tried to argue otherwise, mainly by obfuscating the issue). Of course, all these vaccine samples from the US and UK tested negative for SIVs and for chimpanzee DNA.

Apart from promoting and favouring such misleading research, several speakers at the Royal Society meeting deliberately tried to confuse and obfuscate the history of what had actually happened during the OPV campaigns in Africa. And then came the coup de grace in the form of Professor Weiss’s closing speech. His comments were quite blatantly biased, favouring only the bushmeat theory, and these were the comments that got reported in the press and in scientific journals the world over.

Weiss was also present at the second major origins of AIDS conference, held at the Accademia Nazionale dei Lincei in Rome in September 2001, where, strangely, he was once again appointed to deliver the final summing-up. This time he was even more flagrantly biased, in that he managed to ignore virtually every bit of the new evidence that I and others (such as Luisa Bozzi and Mikkel Schierup) had presented. This time I was so disgusted that I surprised myself by getting up and walking out, shouting at the podium as I did so: “This speech is a disgrace.”

Michael Worobey’s past and future research.

The author of the “Emergence of HIV in the Americas” study is the young Canadian Michael Worobey, a Rhodes Scholar who first worked under molecular biologist Eddie Holmes (another bushmeat proponent) at the Department of Zoology at Oxford University, and who a few years back was appointed head of his own evolutionary biology lab at the University of Arizona in Tucson.

Worobey actually has a significant history of involvement in the origins-of-AIDS debate. Furthermore, he would appear to be the man who is being promoted by kingmakers such as Robin Weiss to become the new “star investigator” of the bushmeat lobby.

The Haitian research may therefore be part and parcel of a continuing process designed to position Dr Worobey in the public eye, and to lend kudos to his work. In reality his Americas paper was not an especially ground-breaking study, but it is one that garners easy headlines – especially when allied to his estimates of when HIV may have arrived in the United States.

And what comes next? This is revealed by the last line of the press release, which states: “Worobey’s next step is following the trail of HIV-1 even further back in time using older archival samples”.

Some clues about what he is actually looking at are provided by Worobey’s 2005 grant proposal to the National Institutes of Allergy and Infectious Diseases (part of the NIH). This ended with his promise to “illuminate the remarkably unstudied early phase of HIV evolution (from around the time of discovery of AIDS, back to 1955 or perhaps even earlier)”.

I consider the fact that Worobey specifically mentions the year 1955, which immediately predates the polio vaccine trials, to be very telling – and in a companion essay to this one I shall explain why such responsible-sounding work is in reality a cause for considerable concern.

Edward Hooper. First version written November 1st, 2007; this updated version written January 20th, 2008; minor changes made and posted on March 19th, 2008.

[See also the essay on “Michael Worobey’s possession of 1950s tissue samples from Stanleyville”, which leads on from this one.]

Contested Testimony in Scientific Disputes: the Case of the Origins of AIDS

Professor Brian Martin, the sociologist of science from Wollongong University, Australia, first entered the origins of AIDS debate in 1991, when he arranged for the publication of Louis Pascal’s seminal monograph on the OPV theory: “What Happens When Science Goes Bad?”. He has never concealed his belief that the OPV hypothesis has not been fairly treated by mainstream Science, and since about 1997, he has given me a great deal of helpful feedback on my work. During the last 15 years he has written a number of essays on origins-of-AIDS – and his sense of fairness and balance, plus his track-record as a defender of free speech in Science, have won the respect of all sides in the debate. At the Royal Society conference in 2000, he made a speech on “The burden of proof and the origin of AIDS” which caused a significant amount of defensive anger among supporters of Hilary Koprowski and the bushmeat theory. In his latest essay on “Contested Testimony”, available here, he examines the question of whose testimony on key issues such as the CHAT campaigns in Africa (that gathered by Stanley Plotkin and associates, or that gathered by Edward Hooper and associates) is more likely to be reliable.

EH 3/11/07

Three Warnings About Potential Future Malpractice by Members of “the Bushmeat Group”

Updated 13/08/06

I trust that my response to Beatrice Hahn’s latest article “The Hollywooding of Science” has not only restored some balance in the “origins of AIDS” debate, but that it has highlighted the flimsy nature of some of the claims that are routinely made by key advocates of the bushmeat hypothesis.

Some of the more common of these flawed claims are that Lindi camp used the “wrong subspecies” of chimpanzee, and that phylogenetic dating analysis “proves” that pandemic HIV-1 existed in the 1930s, long before the polio vaccine trials. Of course, the most common claim of all by the Hahns is that they have “laid to rest” the OPV hypothesis. But not one of these claims stand up to scrutiny.

Continue reading “Three Warnings About Potential Future Malpractice by Members of “the Bushmeat Group””

Beatrice Hahn. A Portrait of Scientific Certainty

Beatrice Hahn. A Portrait of Scientific Certainty: Doctor Strangelove in a Silk Shirt.

Beatrice Hahn is a powerful woman, though she is also one who is possibly feared more than respected or liked. Her method of operating is reminiscent of that of her former boss, Robert Gallo, and indeed of Gallo’s mentor, Hilary Koprowski, before that. She is a control freak, and she demands that all who work for her, or in collaboration with her, toe the party line. This makes it easier to control the outgoing message, and indeed she is a past master (or mistress) of subtly adapting her position in order to “absorb” previous inconsistencies, and thus to glide over her own mistakes. By exerting this degree of control, she is able to make it appear (at least to newcomers to the field) that she and only she is fully in command of the facts.

If it suits Hahn to be treated as the fount of all knowledge on how AIDS began, it probably suits the medical establishment as well, many of whose members are scared stiff by the implications of the OPV theory. Indeed, the scientific establishment is set up in such a way to facilitate an intellectual coup of this sort. Peer review (at least as practised by the major journals) allows a situation in which only views that tie in with Hahn’s are broadcast, which is why Nature and Science have repeatedly published alleged “refutations” of the OPV theory, but have never dared publish an article that simply lays out the theory, so that people can decide for themselves where they stand.

It’s hard to know what summarises this policy better: intellectual cowardice, or intellectual totalitarianism. But predictably, my own latest submission to Science (a 300-word letter of response to the latest claims by Hahn’s team) was rejected without any reasons being offered, or the opportunity to respond.

Indeed, Big Science is increasingly run along capitalist lines, with the grant system making it eminently easy for dissident views to be crushed. It seems that such a system cannot easily cope with an independent researcher like myself, someone who cannot be pressured into silence. That’s why, after themselves being stunned into silence for several months after The River was published, members of that establishment [led by Weiss and Wain-Hobson, and including Plotkin, Hahn, Sharp, and Korber] spent months organising a two-day conference on AIDS origins at the Royal Society, which, though Weiss and Wain-Hobson insisted otherwise, was actually devoted to a carefully-orchestrated attempt to consign the OPV theory to the grave. As it happens, they narrowly failed to carry out their burial plans – but only because I was so disgusted by the way I’d been treated that I elected to carry on with my AIDS researches.

Within six months of the Royal Society meeting I had realised that batches of Koprowski’s OPVs had been locally-made in Stanleyville. It’s now six years later, and at this stage I am ready to state one simple thing. I sincerely believe that the evidence in favour of the OPV/AIDS theory is now overwhelming.

Back to Beatrice Hahn. It’s my belief that the Hahn group’s approach to Science is not dissimilar to the way a giant corporation does business, either crushing different or opposing ideas through superior financing or “weight of numbers”, or else absorbing them quickly and quietly within its own sphere of influence. The work of several scientists (for instance in determining that the SIVs of certain African primates other from chimps feature a vpu gene) has first been submitted to Hahn’s group for checking or refereeing, and then later absorbed, and eventually published under the Hahn imprimatur, with the new revelation lent her own personal bushmeat spin.

Nowadays the official (and surprisingly oft-repeated) party line is that it was Hahn who discovered that HIV-1 had evolved from the SIV of the common chimpanzee. Of course, this is nonsense. The similarities between the two viruses were first reported by Martine Peeters in 1989, and the first chimp SIV sequence was published by Simon Wain-Hobson in 1990. Hahn first published on this subject a decade later, in 1999, when she proposed that it was not just common chimps, but Pan troglodytes troglodytes chimps, which represented the ancestral host. (Though Hahn claims otherwise, this is still unproven.) Nowadays Peeters frequently appears as a Hahn co-author, even if she is one of the few members of that team to inspire confidence, in that she is one of its more thoughtful and less ego-driven members. Wain-Hobson has his own views on Hahn, and although he prefers not to antagonise her, he generally prefers to keep his distance.

All this, of course, helps explain why Beatrice Hahn so hated having to deal with a hypothesis of origin contrary to her own, especially when it was proposed vigorously, and by someone who, in her eyes at least, was a “non-scientist”. Even with the help and compliance of leading journals like Science (where AIDS news coverage seems to be determined mainly by their ubiquitous reporter and bushmeat believer, Jon Cohen) and Nature (the AIDS coverage of which is controlled by another bushmeat believer, Robin Weiss), she has been forced to announce on at least three separate occasions that she has “refuted”, or “laid to rest” the OPV theory of origin. Furthermore, she frequently loses her temper on this topic, and has been quoted as referring to the OPV theory as “bullshit”, and to The River as “that fucking book”. It’s nice to know that her way of dealing with opposing views is so considered and mature!

Later on, being the woman she is, she affects contrition, and says she is worried about how others will view her for her outspoken comments. It takes lackeys like John Moore to reassure her: she is still working on exactly the right lines; she is still loved. (My views on Moore are forthright, but justified: he hands out abuse in spades, so must be prepared to be judged in similar terms.)

Hahn has recently let it be known that she regrets how she treated me when I came to interview her in 1995, when she acted with her customary arrogance, and unwillingness to listen to anyone’s views but her own. [See “The River”, pp 647-652.] This rather hilarious affecting of contrition is both insincere, and very typical Beatrice Hahn. The reason I write this with some confidence is that the last time I tried to contact her in a collegiate spirit, in 2003, was to ask some questions of her, questions which she barely answered. In the course of the e-mail, I floated the possibility that chimp SIVs might have recombined in tissue culture to produce the ancestral strains of HIV-1, and she responded as follows: “You are obviously entitled to having [sic] an opinion and to express that opinion in any way you want, but don’t kid yourself (or others) that you have the necessary scientific background and expertise to make a judgement call in this matter.” Since on such issues I regularly consult a number of scientists whom I consider to have judgement as good as, if not better than, Dr Hahn, I did find this comment to be revealing of how she responds to alternative viewpoints.

(Later, in 2005, I twice contacted one of Hahn’s assistants, Brandon Keele, offering him a little collaborative input about the DRC, and once again asking him about the results of their lab’s SIV testing in chimps in the DRC. He did not even bother to reply. This was not only bad manners, but also worrying. Hahn’s group – and other groups – have been testing DRC chimps for SIV for years now, and yet have reported nothing of their results, other than Michael Worobey’s single sequence of chimp SIV from the Parisi Forest, near Stanleyville, which he and Hahn cynically and misleadingly announced as a “refutation” of the OPV theory. This lack of public announcement only encourages the perception that the reporting of chimp SIVs in Africa may be selective.)

But Hahn’s recently reported “contrition” is also shallow, for it suggests that she believes that I have opposed her for the last ten years out of pique. The real reason, as anyone who follows this website will know, is because I believe that she is rather often a complacent and less-than-rigorous scientist.

Indeed, I think her certainties (most of which involve areas which are anything but certain) are potentially very dangerous.

I am not alone in believing that Professor Beatrice Hahn may be the stuff of nightmares: Bad Science tidily presented,T.(BDoctor Strangelove in a silk shirt.

Here are some of the areas in the origins of AIDS debate where Hahn insists she is right, but where I (on the basis of what I have learnt during the sixteen years that I have spent pursuing this subject) have the temerity to believe that she is profoundly wrong.

These are Beatrice Hahn’s three alleged “disproofs” of the OPV theory.

“Disproof” #1
Hahn and her collaborators have frequently claimed that the chimps used in the polio experiments in Stanleyville/Kisangani were of “the wrong subspecies”, and that this effectively refutes the OPV hypothesis. (Their latest claim that “the source” of pandemic HIV-1 lies in south-eastern Cameroon is only an extension of the same argument.)

But the documentary proof that there was at least one Pan troglodytes troglodytes [Ptt] among the chimpanzee experimentees at the Laboratoire Medical de Stanleyville destroys this argument at a stroke.

In fact, there is new evidence suggesting that Ptt chimps may have been at Lindi camp from the beginning. I am still finding out further details about this, and, if appropriate, will publish more when the time is ripe.

“Disproof” #2
Together with collaborators of hers such as Stanley Plotkin and Hilary Koprowski (the men from the Wistar Institute in Philadelphia who developed CHAT oral polio vaccine, and helped supervise the African trials of that vaccine) Hahn has frequently claimed that representative samples of CHAT vaccine have been independently tested – and found completely free of HIV, SIV and chimpanzee DNA.

Those findings were correct. But unfortunately for Hahn and Plotkin, they did not constitute a disproof of the OPV theory. By mid-2002 I had obtained multiply-confirmed evidence (based on personal testimonies and archival documents) that batches of CHAT vaccine had been prepared locally in Stanleyville, grown in tissue cultures based on chimpanzee kidney cells (and, it seems almost certain, chimpanzee sera).[6]

However, the phials of CHAT vaccine that Stanley Plotkin arranged to have tested all originated from the Wistar, not from the LMS. In short, they tested the wrong batches of vaccine. Of course, as I now realise, Plotkin and Koprowski must have been fully aware of this at the time that they were arranging the testing. But I wasn’t.

Does any of the CHAT vaccine prepared at the LMS still exist? I believe that samples may still exist, and that if they do, they would probably be stored in certain freezers in the USA and Belgium. Will any of these samples ever be released for independent testing? On this one, your guess is as good as mine – though I have a pretty strong hunch that they will not be.

“Disproof” #3
In 2000, Sharp and Hahn (and other collaborators, such as Bette Korber) began claiming that “phylogenetic dating” proved that the AIDS virus had first emerged in about 1931, plus or minus roughly ten years – in other words, more than a decade before the OPV trials in Africa.

Again, it was balderdash. Phylogenetic trees are very useful, and can be expected to be roughly as accurate as human family trees (provided one accepts that the latter occasionally feature some mistakes). But attempting to date HIV-1 by phylogenetic analysis is completely different.

Estimating the rate of mutation of an organism works pretty well for most organisms, or indeed for DNA-based viruses like smallpox. But it does not work for the SIVs and HIVs, which belong to a particular group of RNA-based viruses called retroviruses. In fact, the immunodeficiency viruses are the most recombinogenic organisms (ie the life-forms most prone to recombination) known to medical science. Recombination is ten times more significant than mutation in the evolution of HIV and SIV. And yet phylogenetic dating (which is predicated on a constant “molecular clock”, beating like a metronome) assumes oonly mutation.

The molecular clock approach is inherently incapable of making any allowance for recombination. All the geneticists can do is try to exclude from their analysis any viruses that look as if they might be recombinants. But if those recombinants were formed early in the evolution of HIV-1 (as I believe the key ones were in this instance), then the geneticists are simply unable to identify, or exclude them.

Korber and others have further argued that when they enter the earliest (“1959”) sample of HIV-1 on their graphs, its date is accurately predicted. Once again, however, they are wrong. Multiple evidence, to be revealed in due course, indicates that the famous “1959 sample” of HIV-1 from Leopoldville was actually not obtained in 1959 at all, but at some point between 1960 and 1963. If one takes the latest option (1963) as the true date of this earliest sample (as indeed one must do, failing the appearance of further accurate information), this sequence now falls outside Korber’s 95% confidence intervals, which range from 1934 to 1962. In other words, the date of the first HIV-1 sample is no longer correctly predicted by her method.

In short, the geneticists have not only used the wrong model in their attempts to date HIV-1. They have also used inappropriate measuring apparatus, and have simply crossed their fingers and hoped (or pretended) that it works.

It’s as if Hahn and her friends were using a thermometer or a rain-gauge to try to estimate the speed of one of those huge river-ferries of the 1950s, working its way up the Congo river. I find it rather enjoyable to look over their shoulders and watch as they try to pull off this scientific sleight-of-hand.

But hang on. What’s that? Over there in the shade, behind the wheel-house? Yes, in that cage, isn’t there something moving, something dark? Isn’t it an animal, covered in fur?

EH 26/07/06

The Hollywooding of Science

"The Hollywooding of Science". Beatrice Hahn’s latest SIV sequences from Cameroonian chimps: an alternative interpretation

Updated 5 August, 2006

If you’re new to these issues, read this first.


a) The latest paper by Beatrice Hahn’s team (B. F. Keele, B. H. Hahn et al: "Chimpanzee Reservoirs of Pandemic and Nonpandemic HIV-1") [Reference 1] features claims that they have discovered the source of pandemic HIV-1, the "AIDS virus".

b) However, on the basis of the evidence presented, this claim is unsafe. In fact, more than that, it represents a rash over-extrapolation.

c) The reasons for rejecting Hahn’s claim include the following: (i) less than 1 in 200 of the chimp troops in this part of Africa have thus far been sampled for SIV; (ii) in reality, the new chimp viruses she has found fall far short of being "dead ringers" for pandemic HIV-1, as has been claimed; (iii) there are close physical and biomedical similarities between Pan troglodytes troglodytes (Ptt) chimps and Pan troglodytes schweinfurthii (Pts) chimps, which some believe should be regrouped into a single subspecies; (iv) members of some groups of Ptt cluster genetically with Pts, and vice versa; (v) despite their claims to the contrary, Hahn and co-authors have not established that Ptt (rather than Pts) represents the reservoir of pandemic HIV-1; (vi) furthermore, the closest primate virus ancestor to pandemic HIV-1 may have existed in a chimp troop that is now extinct.

d) The true reason why it is so important to Hahn’s group to establish the Pan troglodytes troglodytes subspecies of chimpanzee as the reservoir of pandemic HIV-1 is that they believe that this refutes the OPV/AIDS theory, which proposes that AIDS began as a result of chimpanzee experiments conducted in Stanleyville, Belgian Congo, in the late 1950s.

e) However, their latest findings do not disprove the OPV/AIDS theory. For a long time, there has been substantial anecdotal and circumstantial evidence that at least some Ptt chimps were present at Stanleyville and/or the nearby chimp camp at Lindi. But a recently-unearthed Belgian article from 1965 proves that the Stanleyville doctors were working with at least one Ptt chimp in early 1960, and perhaps in 1959. Co-caging and group caging were routine at the holding centres at both Lindi and Stanleyville, meaning that viruses could have spread from this Ptt (or similar animals) to other primates (Pts and bonobos) housed in these centres.

f) Furthermore, it is far easier to postulate Ptt chimps, including chimps from south-eastern Cameroon, ending up in the huge holding centres at Lindi and Stanleyville than it is to postulate a human infectee moving from Cameroon to Leopoldville, allowing AIDS to spawn there – and only there.

g) It is also worth emphasising that because of recombination between SIV strains, the origin of pandemic HIV-1 does not automatically require the involvement of the closest viral ancestor genetically. [See below for further details.]

h) There are multiple problems with the latest Hahn/Sharp scenario of how the AIDS pandemic might have started in Leopoldville (over 600 miles by river from her alleged chimpanzee "source"). By contrast, the OPV/AIDS hypothesis is inconvenienced by none of these.

i) The discovery that Ptt were used in the Stanleyville experiments has more significance for the origin of AIDS than Hahn’s latest data from Cameroon. Once again, the claims by Hahn and her buddies that "the OPV theory has been laid to rest" are revealed as empty bluster.

The Major Claims (and Flaws) of the Latest Hahn Paper

The latest paper by Beatrice Hahn’s group about newly-discovered simian immunodeficiency viruses (SIVs) among ten troops of wild chimpanzees from Cameroon was published on line in Science express in May 2006, and in Science itself on July 28th, 2006.[1]

The article elicited considerable media attention, and is notable for several reasons.

  1. The authors report rather high SIV prevalence rates (of between 29% and 35%) among some of these populations of wild-living Pan troglodytes troglodytes (Ptt) chimps. The overall prevalence of SIV among the five troops for which they provide full numerical details is just over 13%, but is likely to be somewhat lower (approximately 10%) among all of the Ptt troops that they sampled. The SIV-prevalence of 10% to 13% in Ptt chimps is slightly lower than the SIV-prevalence of "about 20%" previously reported by the same authors from three troops of Pts chimps living near Gombe, Tanzania.[17]
  2. The authors report that two of the ten chimp troops sampled (both of which came from the south-eastern corner of Cameroon) were infected with SIV strains that were genetically closer to the virus that has caused the AIDS pandemic (pandemic HIV-1, or HIV-1 Group M) than any other previously-sequenced SIVs from African primates.
  3. Surprisingly, the degree of genetic homology between the new chimp SIV strains and pandemic HIV-1 is not reported. All we have is the authors’ rather vague claim that "inclusion of the new viruses [in phylogenetic trees] reduced the lengths of the branches marking the cross-species transmission events for all genomic regions by almost half". Since the previous closest homology between chimpanzee SIVs and pandemic HIV-1 was reported as roughly 80%, this statement would seem to suggest that the degree of homology between these latest chimp viruses and HIV-1(M) is approaching 90%. However, examination of the trees that are published at the end of the article suggests that this is incorrect, for here the degree of homology (especially for the important env, or envelope gene) appears to be considerably less than 90%.
  4. This discovery of a new closest ancestor to pandemic HIV-1 is undoubtedly exciting, but sadly, as so often is the case with Dr Hahn and her collaborators, the manner in which they report it involves a substantial amount of exaggeration. In February 2006, Professor Sharp gave a speech entitled "Where AIDS Came From" to the 13th Conference on Retroviruses and Opportunistic Infections at Denver, Colorado,[2] in which he claimed that he and his colleagues had discovered "the source" of HIV-1. Similarly, journalists who have recently interviewed Professor Hahn (and who have clearly been influenced by her comments) have stated that she has found "the cradle" of pandemic HIV-1, and that the new Cameroonian chimp viruses are "dead ringers" for the human pandemic virus.[5] All these claims are untrue. Hahn’s group has definitely found the closest non-human primate relative to pandemic HIV-1 to be discovered thus far. However, on the basis of the evidence they present in Science express, they have found neither the source nor the cradle of pandemic HIV-1, nor a "dead ringer" for the human AIDS virus.
  5. Keele, Hahn and Co. also assert: "Given these short branch lengths, it is highly unlikely that other SIVcpz [chimp SIV] strains exist that are significantly more closely related to HIV-1 Group M…..than the viruses from [these Cameroonian chimp] communities". This is a sweeping – and almost meaningless – statement, partly because all depends on one’s definition of the word "significantly", and partly because, even if someone were to find a virus that was even slightly more closely related to pandemic HIV-1, this would substantially lessen the impact and import of the present paper. In fact, it might well render the present paper redundant. It is important to note that – as Keele and Hahn themselves acknowledge – there are "vast areas of west central Africa not yet sampled" for chimp SIV – a situation that is even more true for central Africa, and in particular for the Democratic Republic of Congo (DRC, the former Belgian Congo).
  6. Hahn’s team also claims that: "These findings establish P. t. troglodytes as the natural reservoir of HIV-1." Again, this statement is incorrect. On the basis of HIV epidemiological studies, Pan troglodytes troglodytes had already been established as the probable natural reservoir of the minor groups of HIV-1 (Group O and Group N), but it is still unclear which chimp subspecies is the natural reservoir for "pandemic HIV-1" (HIV-1 Group M). Hahn is seeking to transpose the apparently reasonable claims about reservoir made for the minor HIV-1 groups across to the major group, HIV-1 Group M, the "pandemic virus". It is both irresponsible and dangerous to make such sweeping claims for Group M, the virus that is the real focus of everyone’s attention, especially when fewer than 1 in 200 wild chimpanzee troops from west central Africa (Pan troglodytes troglodytes) and central Africa (Pan troglodytes schweinfurthii) have actually been sampled.
  7. To give just three examples of why these claims are over-stated: (a) In 1961, a group of Pts chimps from Mambasa, eastern DRC, was reported which had notably similar blood characteristics to Ptt chimps, 800 miles (as the crow flies) to the west. A genetic link between the two groups was posited.[7] (b) I have photos of young Pts chimps from northern DRC, chimps that were captured by Gilbert Rollais from around Ango and Bondo for use at Lindi camp, that display the "early balding" that the great American zoologist, Jonathan Kingdon, says is typical of Ptt chimps. Once again, this suggests that there might be genetic similarities between Ptt chimps and certain groups of Pts.[14] (c) In 2001 the Swiss primatologist Pascal Gagneux published an article that featured a series of phylogenetic trees which show how the genomes of Ptt and Pts chimps are to a large extent intertwined.[15] Because of this, Gagneux postulated that it was perhaps not legitimate to classify Ptt and Pts as two separate subspecies. Additional background: 57 of the north Congo chimps mentioned in (b) and 21 of the Mambasa chimps mentioned in (a) were among the 400 chimps used for oral polio vaccine (OPV) studies at Lindi camp. This illustrates that these, or chimps from any other part of the 200,000 square mile area that provided chimps for Lindi camp, might represent the true reservoir of pandemic HIV-1. There is also another possibility for, as Gagneux noted, the viral reservoir might have existed in a chimp troop which is now extinct.
  8. The Hahn team, however, seem strangely determined to "prove" that the crucial reservoir, that of pandemic HIV-1, lies as far from Stanleyville/Kisangani and Lindi camp as possible. An example: at the aforementioned Denver conference in February 2006, another of the Hahn collaborators, Fran van Heuverswyn, gave the key paper in which these new Cameroonian chimp viruses were reported. The Webcast of her speech[11] includes some questions asked at the end, and a member of the audience points out that all the studies seem to be from Cameroon, and asks if it is hard to obtain similar samples from wild chimps in the Democratic Republic of Congo [DRC]. She responds: "In the lab of Beatrice Hahn they have analysed samples from the DRC and they were all negative." This claim is untrue, for at least one of the two currently reported chimp SIV sequences from the DRC was analysed in Hahn’s lab, as well as that of Michael Worobey. Furthermore, it is known that people working in Hahn’s lab, notably Brandon Keele, have been analysing large quantities of chimp samples from the DRC over the last couple of years, and given what is already known about the epidemiology of SIV in chimpanzees, it is highly unlikely that none of these samples should have been found to contain SIV. Other teams, too, obtained chimp samples from the DRC several years ago, but no SIV sequences have been reported apart from the sequence from the Parisi forest reported by Worobey and Hahn[16], which they then falsely claimed to have "refuted" the OPV theory. This lack of reporting of chimp sequences from the DRC (and the misrepresentation of the significance of one of the two reported sequences) is now so pronounced that it is cause for some concern. In the light of the known suppression of other data in this heated debate [see "The annexing of the Stanleyville samples" on this website], one has to ask whether data about SIV in Pts chimps could have been deliberately suppressed.
  9. Although Keele and Hahn’s paper is rather brief, it contains several problem areas. However, as with previous papers from the Hahn team, the authors’ response to flaws or snags in their arguments is to gloss over them. The other main shortcomings of the paper include the following: (a) the fact that there is a more than 500-mile distance by road, and a more than 600-mile distance by river, between their alleged cradle of pandemic HIV-1 in south-eastern Cameroon, and the place where they believe AIDS "spawned" (Leopoldville/Kinshasa); (b) the fact that for someone to travel from their "source" to their "spawning-ground" would have required crossing two national boundaries (from Cameroon to Afrique Equatoriale Francaise, AEF, and from there to the Belgian Congo); (c) the fact that there is zero evidence of early AIDS, or early infection with pandemic HIV-1 anywhere near south-eastern Cameroon, or, indeed, anywhere in the intervening area between south-eastern Cameroon and Leopoldville; and (d) the fact that many commentators (including members of the CDC retrovirus team, led by Tom Folks) believe that recombination between different immunodeficiency viruses in humans was the event that sparked the AIDS pandemic. The Hahn group has persuasively argued that chimp SIV originally arose as a result of recombination between two other primate SIVs in the body of a chimpanzee – but that has no relevance for what Folks et al. are saying. The Hahns find it extremely difficult to explain convincingly how the key recombination event or events identified by Folks might have occurred – namely at the time of, or soon after, the transfer of chimp SIV to humans. By contrast, recombination is an intrinsic part of the OPV theory, which proposes that such recombination occurred at the very beginning of the story, both in vivo and in vitro, at Lindi camp and the Laboratoire Medical de Stanleyville, respectively. Each of these issues will be examined in more detail below.

The Bushmeat Advocates Finally Announce How They Think AIDS Began

To my mind, there is one truly valuable thing about this latest article by the Hahns, and it is this. For years, Hahn and her team have kept their hypothesis of the origin of AIDS as vague as possible, which had the great merit (from their perspective) that it could not easily be refuted. But now, for the very first time, they have actually spelt out in print how they think the AIDS pandemic started.

Of course, once a hypothesis is actually on the table, then counter-arguments can be raised against it.

Because they have to weave their account into their favoured hypothesis of origin of AIDS (the bushmeat hypothesis), what they come up with is strangely far-fetched – especially to anyone who knows something of Africa (which Hahn and her supporters, it often seems, do not. Indeed, the word on the grapevine is that Hahn herself is freaked out by the prospect of visiting Africa.)

One of the techniques Hahn frequently uses in her arguments is to present hypothesis and speculation as if it were fact. For instance she claims that this article, and previous articles from her team, "provide for the first time a clear picture of the origin of HIV-1 and the seeds of the AIDS pandemic".

To my mind, this is a reckless over-statement. But for the record, this is the scenario that Hahn and her colleagues propose.

They posit a chimp-hunter or bushmeat-seller who becomes infected with SIV by blood-to-blood contact, probably while butchering or skinning one of the chimps from the south-eastern corner of Cameroon.

They further propose that the cross-species infection of this one person (the index case) single-handedly sparks the AIDS pandemic.

And, still sticking to the tenets of their discredited phylogenetic dating hypothesis, they propose that this happened some time around the 1930s.

They have to presume that this hunter or market-seller, the index case, does not spark any local outbreak of AIDS-like disease in Cameroon or in neighbouring Congo Brazzaville – or at least not one that was recognised and/or reported as an unusual condition by the French doctors who then worked in this area.

And because there is no correlation between the ranges of Hahn’s Cameroonian chimps and the first recorded appearances of HIV-1 (which were exclusively in the Belgian Congo), she and her people have to hypothesise that someone quickly exported the virus, so that it was able to become established in Leopoldville (550 miles to the south-west by road, or more than 650 miles away by river), where they believe that the AIDS pandemic was somehow "spawned".

In fact, their article makes it clear that they believe that the index virus (or its descendants) was/were brought southwards by river. This means that they require that the first human infectee (or someone infected directly or indirectly by them) took at least two steamers down the Sangha and Congo rivers (travelling from Ouesso to Brazzaville to Leopoldville/Kinshasa and crossing two national boundaries in the process), and ended up delivering the virus to Leopoldville.

Hahn and Co. apparently believe that once this ancestral version of HIV-1 had arrived in Leopoldville, the various subtypes of HIV-1 somehow developed – first of all in isolation (presumably within different suburbs of that city!), and then, later, as an epidemic.

Then, at some later time, they propose, the different subtypes of HIV-1 began to meet up in the cells of infectees and to recombine, thus creating the recombinants and complex mosaic strains of pandemic HIV-1 that appear to have existed from, at the very latest, 1976.

So they have to postulate that first diversification and then recombination occurred in Leopoldville – and that all this happened before the various viral strains of pandemic HIV-1, such as the recognised subtypes, began to be exported outwards and around the world.

In other words, there are many rather substantial difficulties to their "chimpanzee bushmeat" hypothesis of origin.

However, as I shall show later, few if any of these problems apply to the hypothesis of origin that they all so dogmatically reject: the oral polio vaccine (OPV) hypothesis.

The Serological Evidence

The available serological evidence does not offer any support whatsoever to Hahn and Sharp’s thinking. In fact, it runs quite strongly against it.

Here is a quick review of the relevant evidence that I have in my files, augmented by information from the excellent HIV/AIDS Surveillance Database, published by the US Bureau of Census.

In 1975-8, blood was taken from 340 pygmies (the greatest of all bushmeat hunters) from the borders of Congo Brazzaville and Central African Republic (CAR), who live just 100-150 miles to the north-east of the suspect Cameroonian chimps. Not one of these samples was found to be HIV-1-positive. Further surveys were conducted in CAR in 1986 among 280 members of the general population in Sangha region (which extends to as close as 50 miles from Hahn’s chimps). Again, not one positive. Another much larger survey was conducted in 1984-7 among 782 pygmies from Sangha region and Lobaye region (immediately to the east), again without a single HIV-1-positive.[9] This evidence strongly suggests that no HIV-1 derived from the Cameroonian chimp troops ever escaped northwards up the Sangha river, into the south-west of Central African Republic or northern Congo Brazzaville, despite the fact that there appears to be quite a heavy traffic of small boats on that part of the river. If Hahn and Sharp are right in their assumption that this south-eastern corner of Cameroon is the source of pandemic HIV-1, then these wholly negative findings are, to say the least, surprising.

So what about Cameroon itself? The south-east of Cameroon has such sparse population that little if any HIV-1 sampling has been done here. But a 1990 study of 125 pygmy adults from Djoum, in the south of Cameroon, but 200 miles west of the suspect chimp troops, found that just 2 were (1.6%) were infected with HIV-1. (It has been proposed that these two infections might have been the result of a pygmy travelling to a local town, having sex there, and later infecting another member of his group; in other words, that HIV-1 was imported from an urban area.) However, 1.6% is a fairly typical prevalence of HIV-1 for a rural area in 1990 in this part of sub-Saharan Africa.

There is therefore no serological data to encourage the Hahn/Sharp hypothesis in Cameroon itself. So let’s look southwards, to Congo Brazzaville, which, indeed, is the country to which Sharp and Hahn hypothesise that HIV-1 "escaped", before ending up in Leopoldville in the Belgian Congo.

A large town, Ouesso, is situated on the River Sangha, just over the Cameroonian border in Congo Brazzaville, and some 30 to 50 miles south of the suspect chimp troops. Unfortunately, it seems that only a single HIV-prevalence survey has been conducted in Ouesso, and that quite late in the epidemic: it involved a survey of 300 pregnant women conducted in 1992, as part of a sentinel surveillance programme. 16 (5.2%) women were found to be infected with HIV (though the type, ie HIV-1 or HIV-2, is not recorded, which raises questions about the specificity of the test). To give some perspective, this is exactly the same HIV-prevalence as that encountered the previous year (1991) among 300 pregnant women in Impfondo (a much smaller town on the Oubangui river, 140 miles east of Ouesso, but inaccessible from there – and indeed, inaccessible by road from the outside world – due to impenetrable swamps). And it is much less than the HIV-prevalence of over 10% already being encountered in the capital, Brazzaville, by the mid-1980s.

In short, that 5.2% HIV-prevalence among typical sexually active adults (pregnant women) in Ouesso in 1992 represents a low to average HIV-prevalence for that year for an urban area in that part of sub-Saharan Africa. (Furthermore Ouesso is on a river, which increases transport links, and normally leads to higher HIV-prevalence.) It’s worth noting that there was a lower HIV-prevalence (2.6%) encountered in the same year (1992) among 300 pregnant women in the smaller town of Owando, 150 miles south of Ouesso on the road to and from Brazzaville, at the point where the two-lane highway begins.

I should perhaps add that the first evidence of HIV-1 in the city of Brazzaville itself is not until 1981, which is two decades after the first evidence of HIV-1 in the Belgian Congo (later Zaire; now the Democratic Republic of Congo). There was one intriguing and fatal case of cryptococcal meningitis (CM) with gastric candidiasis in an 18-year-old woman living in the city of Brazzaville in 1958, conditions which, on their own, might be considered suggestive of AIDS. However, the appropriate antibiotics were only given to the patient in "modest" doses for a brief period, and she also suffered from severe anaemia and an "extremely brutal hepatitis". It is therefore likely that the latter diseases (and the less than adequate therapeutic regime) precipitated the CM, rather than any HIV infection. In short, there is no serological or clinical evidence from Congo Brazzaville to support Hahn’s hypothesis of AIDS origin.

There is also some important and relevant recent data about SIV-like infection (rather than HIV infection) in humans. In the last few years, two American scientists, doctors Burke and Wolfe, have made an exhaustive search for evidence of SIV-like infection among hunter-gatherers from different parts of Cameroon (but almost exclusively from the south). It is reasonable to surmise that this study might have been connected to the Hahn research. However, they did not find a single SIV-positive sample among the 76 plasma tested. They found a host of other viruses, including several infections with a foamy virus which, like SIV, is a simian retrovirus. But they found no SIV.

Burke and Wolfe also tested 1,224 plasmas from a general population coming from urban and rural areas of Cameroon, where people "may handle [primate bushmeat] but are unlikely to have repeated contact with the blood or body fluids of freshly killed animals". Just one single plasma showed some indications of exposure to SIV (in this case SIV from a colobus monkey) by one of the assays used (ELISPOT), but the result was hardly convincing, for the plasma in question showed only weak cellular reactivity, and the authors were unable to amplify any SIV nucleic acids. Because other assays did not give positive results, this might have been a false positive, or it might be that they had genuinely detected one single human exposure to SIV in over 1,300 plasma, but that this exposure had failed to cause any productive human infection.

Burke and Wolfe’s research, which appeared to be specifically designed to obtain data that lent support to the bushmeat theory of origin, actually did the exact opposite. There is still no data that directly supports the hypothesis that hunters can become infected with chimpanzee SIV through the handling and butchering of chimpanzee bushmeat.

None of the above data encourages the perception that HIV-1 was spreading southwards from south-eastern Cameroon, or Ouesso in Congo Brazzaville, to Brazzaville and Leopoldville at any point in the early twentieth century. In fact, there is not one jot of serological or clinical evidence that offers support to the Hahn hypothesis.

However, this is not what Hahn’s principal collaborator, Paul Sharp, thinks. In a recent interview with Ed Susman of UPI, Sharp proposed that "there were probably thousands of people in the region" between Cameroon and Kinshasa who were already suffering from AIDS by 1959.

This is clearly an absurd claim. But if nothing else, it serves to demonstrate the frequently superficial nature of Sharp and Hahn’s arguments, especially when they move outside their designated fields.

To borrow the words of a scientist who works in the same field, and who knows their work well, this type of analysis represents the "Hollywooding of Science".

It’s extremely good that, after years of prevarication, the members of Beatrice Hahn’s group have finally spelt out what they believe in. Because, as it turns out, their scenario of transfer and early spread, far from being the "clear picture" that Hahn claims, is in reality confusing and confused.

Instead of providing a clear history of "the origin of HIV-1 and the seeds of the AIDS pandemic", the scenario they advance is quite remarkably difficult and far-fetched.

I (and several scientists I have spoken with in the last few weeks) believe that Hahn and Sharp have got it wrong.

Their new chimp viruses are the closest yet to pandemic HIV-1 viruses, but they are not that close!

For them to claim, without supporting evidence, that it is "highly unlikely that other [chimp SIV] strains exist that are significantly more closely related to HIV-1 Group M…..than the viruses from [these Cameroonian chimp] communities" shows that their analysis continues to be highly speculative, especially when they have only fairly recently started sampling wild chimpanzee troops for the presence of SIV. (In fact, I believe they began their studies only after my late friend and collaborator, Bill Hamilton, had begun his similar researches around Kisangani in the DRC.)

Despite their latest efforts in Cameroon, which are indeed commendable (unlike their reporting of them!), less than 0.5% (or 1 in 200) of the chimpanzee troops in west central or central Africa have thus far been sampled. [This is my own estimate, calculated on the basis of current chimp population estimates and average troop sizes.]

Hahn and Sharp’s findings thus far do not provide the source of the AIDS pandemic. And neither do they establish Pan troglodytes troglodytes (rather than Pan troglodytes schweinfurthii) as the natural reservoir of pandemic HIV-1….though they would like you to believe otherwise.

My own gut feeling (and those of several persons I have discussed this with) is that the "closest ancestor" to pandemic HIV-1 has not yet been found, and that it may be located some significant distance from south-eastern Cameroon.

If I had the money and resources that are available to Hahn’s team (which is backed not just by US government grants, but by a $500,000 no-strings-attached "Distinguished Achievement Award" grant from Bristol-Myers Squibb), the chimpanzee troops that I would be most eager to sample as part of a search for a "closest ancestor" would include the following: Ptt troops from the Mayumbe region to the west of Kinshasa, (the one area in the Democratic Republic of Congo where Ptt chimps are found); Ptt troops from the region west of Ouesso, in northern Congo Brazzaville, in other words from the area directly to the south of Hahn’s Cameroonian chimps; Ptt troops in Haute Sangha region, in the extreme south-western corner of the Central African Republic; Ptt and Pts troops from either side of the Oubangui river, in Congo Brazzaville and DRC respectively; Pts troops from the savannahs of northern DRC (around small towns like Ango and Bondo); Pts troops from eastern DRC (from around Mambasa); and Pan paniscus troops from the region to the south of Kisangani. Plus several places in between! (No reports of the SIV testing of any of these troops of chimps or bonobos have thus far been published.)

One last point before moving on. Because of the role that recombination may have played at the very beginning of the AIDS epidemic, the genesis of pandemic HIV-1 may not necessarily even require viral transfer to a human of the closest ancestral SIV strain from a non-human primate. [For that argument, see below.]

An Alternative Explanation of the New Data

At this stage I shall attempt a different approach. What I propose to do is to treat Hahn’s claim that she has found the source of pandemic HIV-1 in south-east Cameroonian source as if it were true, and use it to advance what I believe is a far more viable hypothesis of how AIDS began than the one that she and Paul Sharp propose.

At least this hypothesis will be supported by known historical and scientific facts.

What this will, I hope, demonstrate is that Hahn’s latest findings are at least as supportive of the oral polio vaccine (OPV) theory of AIDS origin as they are of the bushmeat theory…if not more so.

In order to make this work, I need to tell a story that, though it is moored in factual accuracy, is purely a work of the imagination. For this reason, the following section of this paper appears in italics, in order to underline that it is fiction, not fact.

Imagine that it is 1956. Imagine that five young Pan troglodytes troglodytes chimpanzees have been captured after a successful hunt by a group of pygmies in south-eastern Cameroon.

The young chimps (alive, but very frightened, for they have just witnessed the adults in their troop being slaughtered, one after the other) are bound at their wrists and ankles and hung loosely on poles. Then six of the young pygmy men set off on a long walk through the forest, towards the town of Ouesso, some forty miles to the south. Before the first day is over, one of the chimps has died. Two of the pygmies turn back with the animal’s body, which will doubtless go in the pot when they rejoin their families. The other four pygmies march on, carrying the surviving chimps – a pole on each shoulder.

On the second afternoon, they reach the Ngoko river, which they cross by a dug-out canoe that is paddled, conveniently enough, by some friends of theirs. And at the end of the second day’s march, they arrive at the edge of the forest, and can see the eery electric glow of the town or Ouesso ahead of them.

In 1956, Ouesso is a thriving place of over 30,000 people. It is also an important trading centre for palm products, rubber, animal hides and mahogany. Furthermore, it is a border post, and the northern terminus for year-round steamer navigation on the Sangha river.

Even though Ouesso is situated in a different country, Afrique Equatoriale Francaise (AEF), some of the young pygmy men know it quite well, for it is their habit to come here when they have something to sell to the townspeople. It is the only town or village of any size in the region. They have nothing like official papers, so their presence here, strictly speaking, is illegal. But it is now dark, and they have little difficulty in flitting out of the forest and into the fringes of the town. Here they know a Moslem man, Abdullah, who runs a small shop, and who is one of the few local traders to allow pygmies into his store. Abdullah knows that some of the French people in Ouesso like to keep chimpanzees as pets, and so he’d previously mentioned that he might be interested in buying a couple of young chimps. He had perhaps not expected four of them to be delivered just a few weeks later!

Abdullah gives the leader of the pygmies some salt and tobacco, and also a small handful of CFA francs, the local version of French francs. He lets two of them stay in the yard behind his shop, telling them to keep the young chimps fed and watered. And in the morning he leaves the shop in the hands of his son, and sets off to try to find some buyers for the chimps. However, he returns that evening tired and dispirited, having failed to interest even a single European in taking on a new pet. What is more, one of the chimps now appears to be poorly, after the trauma of the long journey through the forest.

Abdullah makes a decision. During the day, he has heard some rumours filtering up from down south of Belgians who want to buy young chimps. His son, Salah, is already booked to set off down the Sangha river on the steamer that leaves in a few days’ time; he is delivering a shipment of mahogany poles to a place on the main thoroughfare in the region: the River Congo. Abdullah asks his son if he will take the chimps with him, and try to sell them on. Salah agrees, and he asks the pygmies to go back to the forest, and to bring some wood to make cages.

While all this has been going on, the other two pygmies have been enjoying themselves. Although not used to money, they have adapted rather quickly to the freedoms it provides. They make a few small purchases to take back to the forest, and they find a place to stay, not far from Abdullah’s yard. They also find some female company, young women who are descendants of Bantu/pygmy unions in the past. By the second night, neither of the two pygmy men sleeps alone.

[At this point, let me cut across to the other hypothesis, Hahn’s hypothesis, for a moment, and imagine that one of the pygmy hunters has been scratched rather badly during the hunt, and in the process, has unknowingly acquired a chimpanzee virus, an SIV, that has infected his blood-stream. My question to Beatrice Hahn is this. Ouesso is a large town, just two day’s journey on foot from where her chimps are living in the forest. Once that virus, that chimp SIV, has – as she postulates – infected a local hunter, and once that hunter has arrived in Ouesso and, as her hypothesis seemingly requires, has passed it on to someone else in that town through sex, is it really likely that these events would not have sparked an outbreak of HIV infection then and there? (Ouesso is the one conurbation of any size in this region. On both sides of the border around Ouesso all is thick forest, but the fact that the Sangha is navigable for steamers as far north as the town makes this the effective entry and exit point to the region for humans. The other relevant detail here is that the local hunters in south-eastern Cameroon are almost all pygmies, and pygmy hunters from Cameroon – or in fact rural Cameroonians in general – would not themselves be travelling down to Leopoldville in the colonial era. Therefore, if one adopts the Hahn scenario, the virus does apparently need to be passed on in Ouesso.) So, to sum up, if Hahn’s hypothesis is correct, why do we not see an eruption of HIV-1 infection in Ouesso, or somewhere a little to the south of Ouesso, at around the same time – or before – the eruption in Leopoldville? And remember: Hahn believes that the virus actually arrives here in the 1930s, not the 1950s. Yet we see no trace of HIV-1 in the vicinity of Ouesso until the 1990s.]

At this point let us leave the pygmies behind. Abdullah and Salah are now the owners of two rough wooden cages and four young chimpanzees, (for the sickly chimp has started eating, and has quite suddenly regained her health). A few days later the chimps, now packed two to a cage, are carried down to the docks on a cart, and then loaded on board the steamer. Over the next two days they and Salah are transported slowly down the Sangha river, as it weaves to and fro through the swamps, eventually to debouch almost 300 miles later into the River Congo, which is this point is a much vaster river, roughly five miles across from shore to shore.

On either side of the Sangha’s mouth there is a small steamer station and customs post – the downstream one at Mossaka, and the upstream one at Loukolela. Salah is heading for the latter, where he is selling his mahogany to a Frenchman who owns a small woodyard. The Frenchman doesn’t want to buy any chimpanzees, but he passes Salah on to an African friend of his from the Belgian Congo, Joseph, who is visiting Loukolela unofficially for a couple of days. A deal is struck, and Salah is relieved and happy, for he knows that he has more than doubled his father’s money.

By contrast with the Sangha junction a few miles downstream, the River Congo at Loukolela is at its narrowest point for hundreds of miles in each direction, and there is a constant flow of traffic across the river to a small port in the Belgian Congo with an almost identical name: Lukolela. This is where Joseph is normally based, and where he makes a decent living dealing in a range of goods, ranging from beer to bicycles. He waits until night has fallen, and then, accompanied by the four chimps in their cages, he crosses the river in a small boat. Joseph knows something that Salah doesn’t, for news passes up and down the Congo as fast as the flow of the huge brown stream. And word has filtered down from Stanleyville that there are doctors in that city who are willing to pay a good price (in African terms) for chimpanzees; to do what with, no-one knows nor cares. By Friday morning, Joseph is to be found sitting at a table at his favourite river-front bar, and occasionally scanning the horizon downstream.

Every week during the fifties, every Friday, the huge Otraco river steamer, with its several barges linked behind, calls at Lukolela on its long journey eastwards towards Stanleyville, where it arrives the following Wednesday. For those five days, as the many-jointed ferry chugs its way through the rain forest, it is a floating city of people, animals and cargo. The Europeans travel in segregated luxury aboard the main steamer, but the Africans have to sleep where they can on the decks or in the bowels of the barges behind. Those barges have everything. They have bars selling local brews; they have tiny restaurants; they have live animals and smoked animals that are brought out in dug-outs from both shores and sold for food – or (in the case of the live ones) as future food, or as pets. And they even have their own discreet red-light district, where a man can purchase the services of a woman for five minutes, or for longer if he chooses. The prostitutes entertain dozens of men each day, and this is an era long before condoms, at least in African society. Officially, the Belgians are very strict about controlling sexual activity and the spread of venereal disease. Unofficially, the captain and crew tend to turn a blind eye to what goes on aboard the African barges.

(Much later, in 1983, the wonderful American writer Helen Winternitz took the same journey by river-steamer up the Congo river from Kinshasa, formerly Leopoldville, to Kisangani, formerly Stanleyville. And she wrote a book about it: "East Along the Equator"; [The Bodley Head/Sceptre: London, 1987]. On pages 74-75 of the paperback edition, she writes about the death of a child passenger, "a sickly boy who had been too thin for too long". Winternitz ascribes the death to malnutrition, but the boy’s mother was working as one of the on-board prostitutes, and it is hard to imagine that she had been unable to afford to feed her child. This moment in 1983 was just before the recognition that there was an AIDS epidemic in Africa, and I think the account is rather significant. The tale is recounted as something rather unusual; there is no recognition of a new disease, a new pattern. If AIDS had already been "spawning" in Leopoldville/Kinshasa for fifty years – as Hahn and Sharp and Korber believe it must have been – then surely it would have emerged onto the world stage before then, and one of the first places for it to emerge would surely have been aboard one of the great Kinshasa-Kisangani ferries, with their populations of thousands. To sum up: this sad death of a prostitute’s child in 1983 was probably not the first AIDS death on board one of the great river-ferries. However, given the lack of interest or recognition it aroused, it sounds as if it might have happened relatively early in the epidemic, rather than fifty years into it. Remember, when AIDS first arrived in the Rakai district of south-western Uganda, it was immediately recognised as a new condition by local people, and given a new name: "Slim".

But back to Joseph and the chimps. On the Wednesday, just before noon, the steamer swings slowly into its final destination – the docks in Stanleyville. By this time the chimps, still in their cages, but well fed and watered by their new owner, have travelled just over a thousand miles from their forest of origin in south-eastern Cameroon. They have been carried upside-down through the forest on poles, they have travelled on board two steamers, and (though they don’t know it) they have crossed two national boundaries.

To Joseph’s relief, it turns out that the rumours are true. As his two cages are unloaded, he is approached by a European man, who immediately begins negotiations. The man from Loukolela tries to hold out for a higher price, but the European (another Frenchman, it seems) starts to walk away, and Joseph has to call him back. A minute later, the chimps have been sold on again, this time for the princely sum of 500 Belgian francs each – the equivalent of about ten American dollars a head.

The next day, the Frenchman, who is named Gilbert Rollais, takes the four young chimps on their final journey. It involves a 20-minute drive by Land-rover, followed by a 500-yard ferry-trip across the Lindi river, and then a further one mile hike to reach a place that has only just been created in the rainforest, after four months of bulldozing and construction. The Africans know it as "Camp Polio", but Rollais and his Belgian doctor friends call it Lindi camp.

The young chimps are needed for some important research that the director of the local medical lab in Stanleyville, Ghislain Courtois, is undertaking into poliomyelitis. Courtois is apparently working with an American scientist too, a man called Professor Koprowski. Rollais has been told that they need as many chimps as he can supply, though he is not entirely sure why this is, given that the polio research of Courtois only seems to require a handful of animals.

Once inside Lindi camp, Rollais takes the chimps to one of the two large hangars, with its walls built of local sticks and mud, blended with banana leaves, and inside which there are forty newly-constructed iron cages. Then the African keepers put each of the four young chimps inside a different cage. The two pairs of young chimps have got used to each other’s company during their long safari, and separating them causes screams of distress. But Rollais orders that each chimp be given a new cage-mate – this being one of the chimps or bonobos that he’s already collected during his hunting expeditions near Banalia and Ponthierville, on the northern and southern sides of the Congo river. He knows that when the young chimps arrive in the camp, they are usually frightened, upset, and off their food. He finds that the best way to persuade them to eat is to give each new chimp a cage-mate, an animal that is already familiarised, and which can show the newcomer how easy it is to eat the unusual foods, like sugar-cane, that the keepers push between the bars. Admittedly the chimps tend to fight a bit to begin with. Often they have to swap them around a couple of times before they find two animals that get along. By doing this, Rollais and the Belgian who runs the camp, Robert Daenens, have managed to prevent any fatalities.

Later, when the newcomers are relaxed, he will arrange for them and their cage-mates to be put in the "play-cage", which is twenty feet long, ten feet high and ten feet deep. The young chimps love that; they play and groom each other, and fights only happen quite rarely.

Though not himself a scientist, Gilbert Rollais knows a bit about chimp taxonomy. He knows that most of the chimps in Lindi are from the two species local to Stanleyville. These are Pan troglodytes schweinfurthii (the local subspecies of chimpanzee from the north bank of the Congo river), and Pan paniscus, the pygmy chimpanzee or bonobo from the south bank. Just three years earlier, Rollais was employed as the chief animal catcher in AEF, a job which he had done since 1949. He made several expeditions up to Ouesso and its neighbouring forests, and is well aware of how abundant chimpanzees are in those regions. That’s partly why he had put out the word that he and his colleagues in Stanleyville were looking for young chimpanzees from any source. So he was not at all surprised that chimps from AEF – and even Cameroon – were beginning to turn up at the Stanleyville docks.

A few weeks after this, an unusual epidemic begins going round Lindi camp, killing many of the chimpanzees. One of the doctors from the laboratory, a man called Osterrieth, swiftly diagnoses it as being caused by an organism known as Klebsiella pneumoniae. The disease kills forty of the bonobos and a few of the common chimps in the space of three weeks. Rollais is told that he needs to get hold of replacements just as fast as he can. The following Wednesday he is back down at the docks, awaiting the steamer from Leopoldville.

Which Scenario Better Fits the Facts?

Of course the story that appears in italics on the last few pages is a dramatised account…even if the factual details that underpin it are accurate, having been based on careful research over several years. I do not normally employ drama or fiction as a way of getting my point across, but on this occasion it seemed justifiable. The reason? To point out just how much more plausible this scenario of origin is than the Beatrice Hahn scenario.

Of course, Hahn thinks the opposite. In a recent National Public Radio (NPR) broadcast in the US,[10] Hahn is quoted as saying that her new evidence about south-eastern Cameroon "lays [the OPV hypothesis] to rest". The commentary continues: "If the vaccinators did use chimp kidneys to make their polio vaccine in a Congolese lab near what is now called Kisangani, Hahn says [they] would not have been of the subspecies that harbors the pandemic virus ancestor." Hahn adds: "Well, you would have to come up with a pretty convincing scenario that would explain how chimpanzees or the viruses from the south-eastern corner of Cameroon end up around Kisangani."

That, of course, is what I have just tried to do (though my drama of the caged chimps, as it happens, was written some days before Hahn’s thoughts were broadcast on NPR).

So let’s compare the two hypotheses. I believe that Hahn has to propose a series of quite far-fetched events.

Firstly her chimp-hunter cannot afford to infect more than one or two people locally, in or around southern Cameroon or Ouesso; for had he done so, then there surely would have been some evidence of an early disease outbreak in that region. Instead he (or someone infected directly or indirectly by him) has to up sticks and travel more than 600 miles, across two national boundaries, to end up in Leopoldville. Once arrived in Leo, he (or she) has to infect other people with the newly-acquired chimp virus. But for Hahn’s idea to work, this new virus needs quickly to diversify, and to create separate strains that are genetically quite distinct from each other – including the strains that are now called the HIV-1 Group M subtypes (A to K). Later, these subtypes have to meet up in the bodies of infected persons and to recombine, in order to create recombinant and mosaic forms of the virus. And only then can any of these early strains of HIV-1 begin to escape from Leopoldville/Kinshasa, and to spread elsewhere in the Congo, and across to Rwanda and Burundi, where their presence can be recognised retrospectively from the 1970s onwards. All of these rather far-fetched things need to happen for Beatrice Hahn’s scenario of origin to come true.

By contrast, look at the story of the caged Cameroonian chimps. Just like Hahn’s story, it requires movement across national borders on at least two occasions. But to my mind, it would have been easier for chimps to have been moved in this way during the colonial era than for colonised Africans to have done the same. I would accept, however, that one could argue that particular point either way. So let’s leave that aside, and instead look at the rest of the two scenarios, which at this point begin to diverge markedly.

For Hahn’s scenario, the means of transport (the ferries) was there, but the "magnet" was not there, for it’s hard to argue persuasively that during the 1930s Leopoldville would have been of any interest to Cameroonians, or to people from the northern end of the AEF territory of Moyen-Congo (now Congo Brazzaville).

For the "caged chimp" scenario, the means of transport (the ferries) was there, and the "magnet" was definitely there: the fact that in the 1950s Koprowski and Courtois and the designated "chimp-catcher", Rollais, were desperate to procure common chimpanzees (ie Pan troglodytes, of whichever subspecies) has been revealed in contemporary documents, and reported by three different witnesses (including Rollais himself). Witnesses from the 1950s (and, indeed, from the 1980s) report that chimps were regularly brought up to Stanleyville/Kisangani on the river-steamers, to be sold at the docks. In the second half of the 1950s, this process is likely to have been accelerated, because the LMS doctors were known to be paying good money for them.

But is it possible to prove whether there were any Pan troglodytes troglodytes among the chimps present at Lindi camp? The one significant published paper [13] by any of the protagonists about the capture and maintenance of the chimps and bonobos of Lindi camp was written by Ghislain Courtois, and published retrospectively in 1967, and it fails to give a definitive answer to the question. Courtois begins by describing the three chimp species or subspecies that were to be found in the old Belgian Congo: Pan troglodytes troglodytes (around Tshela in the far west), Pan troglodytes schweinfurthii and Pan paniscus. Having provided a sketch-map of the three ranges, he writes the following: "In view of the position of Stanleyville, and the geographic ranges of the different species, we were therefore able to make our choice from Pan troglodytes schweinfurthii (Pts) or Pan paniscus (Pp)." Elsewhere in the article he writes: "these were the two varieties of chimpanzees…that could interest us". The somewhat ornate phrasing is interesting, and it is noticeable that on both occasions it allows Courtois to avoid specifying whether or not any Pan troglodytes troglodytes were present in the camp.

But if Ptt chimps had been present, why might he have wanted to avoid mentioning such a thing? Well, we know that many of the Lindi apes died soon after arrival in the camp from Klebsiella pneumoniae, and that even back in those days the Stanleyville doctors concluded that the Klebsiella infection had probably been facilitated by some prior viral invader; they apparently suspected an adenovirus. Nowadays, Klebsiella pneumoniae is well-known as an opportunistic infection that has frequently appeared during outbreaks of simian AIDS, following the cross-species transfer of SIV in American primate facilities. This suggests that SIV (especially one that crosses from one subspecies or species to another, which would be expected to impact on viral pathogenicity and infectivity) would have been an extremely good candidate for the mystery viral invader. 1967 was long before anyone knew of the existence of SIVs. But is it possible that Courtois, even with his fairly rudimentary viral knowledge, might have deduced what was going on? If so, it might be that by the time he wrote the 1967 paper, Courtois had guessed that the presence of "non-indigenous chimps" at Lindi camp might have been the source of the viral problem – and therefore decided that any mention of Ptt at Lindi would be a detail that was better omitted.

Apart from this, the records of Lindi camp are extremely sparse, and only provide details about 54 chimps, or 13.5% of the 400 unfortunate animals that were "used" [their term] in the polio programme.[3] But from those records, we know that one chimp from Coquilhatville (now Mbandaka, just upstream from Lukolela) was present at Lindi camp from April 1957 onwards, and that (rather unusually) she was still alive two years later. Furthermore, it seems from the experiments that were conducted on these animals that all 54 of them were Pan troglodytes (common chimps) rather than Pan paniscus (pygmy chimps or bonobos). Because the district around Coquilhatville faces the ranges of both Pan troglodytes subspecies, Ptt and Pts, on the opposite bank of the Congo river, it is clear that the Coquilhatville chimp could have been either a Pan troglodytes troglodytes or a Pan troglodytes schweinfurthii. But that is still somewhere short of proof.

However, in recent weeks dramatic new evidence has emerged that provides the hard proof that had previously been lacking. I recently located a medical paper which reveals that the Laboratoire Medical de Stanleyville doctors were indeed experimenting with at least one Pan troglodytes troglodytes chimpanzee.[4] Other published and unpublished papers in my possession reveal some of the prior history of this Ptt chimpanzee. They reveal that it (and seven Pts chimps) were part of a group of sixteen chimpanzees which were obtained by Gilbert Rollais between August 1959 and February 1960. They were apparently not involved in the polio or hepatitis experiments, but they were used in atherosclerosis experiments beginning in the latter month. We know that Lindi camp closed in January 1960, and that at that date the surviving Lindi chimps, numbering about 60 in total (and including all, or most, of the subset of 16), were transferred to a hangar immediately behind the Stanleyville laboratory, the LMS, and that this hangar became the main chimpanzee holding centre from that point on.

It is therefore likely, but not certain, that the Ptt chimp spent at least a few months at Lindi camp before it closed. But in any case, whether this particular chimp ever stayed at Lindi camp, or only arrived at the LMS in February 1960, is unimportant. The vital thing is that it is now proven that the LMS doctors included some Pan troglodytes troglodytes chimps (perhaps even some from Cameroon!) among their experimental animals.

The question of the sources of the chimps at Lindi and the LMS is vitally important, because viruses from those chimps might have been spread throughout the two facilities. This is because co-caging of chimps was routine at both Lindi and the LMS, and in both places the chimps and bonobos were allowed to play together (at Lindi in a large group cage). Several witnesses have reported that there used to be frequent fights between the animals, and thus the ideal conditions were created for onward transmission of viruses such as chimp SIVs, at both venues.

But which chimp SIV strains might have been passed on? Beatrice Hahn wants to insist that the presence in Stanleyville of Ptt chimps (and indeed, of south-eastern Cameroonian Ptt chimps) is necessary for the OPV theory to remain viable. (And because she believes that no Ptt chimps were present in Stanleyville, she argues that her latest findings repudiate the OPV/AIDS theory.)

I do not concur with Hahn’s analysis, not least because, as previously explained, I am far from convinced that she has established Ptt as the reservoir of pandemic HIV-1, or that she has identified the true "source of pandemic HIV-1" in south-eastern Cameroon. But in any case, we now know for certain that at least one Ptt was present among the experimental animals in Stanleyville – and the presence of that one chimp disposes of Hahn’s argument. (In reality, of course, it is likely that there were more Ptt chimps in Stanleyville than just this one.)

In addition, I have several further documents (both from the 1950s and the modern era) that are relevant to this important subject. I am still seeking confirmation of certain important details, so I shall not attempt to include this further information now. Suffice it to say, however, that additional details about the chimpanzee subspecies housed at Lindi and Stanleyville are likely to be forthcoming at a future time.

The Recombination Factor

In 2004, a CDC team led by the head of the retrovirology lab, Tom Folks, published an excellent article entitled "Recombinant Viruses and Early Global HIV-1 Epidemic."[8] They had tested nearly 4,000 serum samples originally obtained in the early to mid-1980s in Kinshasa. Folks’s team found that all of the major subtypes of HIV-1 were present, and that 37% of all HIV-1-infected sera showed evidence of recombinant or multiply recombinant (ie mosaic) HIV-1 viruses…an apparently extraordinary finding for so early in the epidemic.

They concluded their abstract: "We propose that the HIV epidemic was well established in central Africa by the early 1980s and that some recombinant viruses most likely seeded the early global epidemic." [My italics.]

It will be recalled that Leopoldville/Kinshasa is not only Professor Hahn’s chosen "spawning ground" for HIV-1; it was also one of the main venues for CHAT vaccination in the late 1950s. Indeed, it is my belief that Leo/Kinshasa was one of several spawning grounds for AIDS, not the only one.

However, for Hahn’s "infected chimp-hunter" scenario to achieve this level of HIV-1 diversification by the early 1980s is very difficult indeed. Basically, her index virus (the one that arrived in Leo with the chimp-hunter, or someone infected by the chimp-hunter) has first of all to diversify, for some reason, into a whole host of different viral subtypes. And then those subtypes have to start recombining on a massive scale. Indeed, it seems that all this has to have happened before any of these viruses starts arriving in other venues – something which we know had begun happening by 1976 at the very latest.

(Strangely, though, the only other places in Africa to become infected with pandemic HIV-1 during the years up to 1979 seem to have been former Belgian territories – like elsewhere in the Democratic Republic of Congo, and 1,000 miles to the east, in Rwanda and Burundi. Hahn cannot explain why those early HIV-1 viruses did not escape north (to Congo Brazzavile, Gabon and Cameroon) or south (to Angola) before the 1980s, but only to old Belgian colonial holdings. I propose that it’s because only the Belgian territories were vaccinated with Koprowski’s OPV, CHAT.)

But let me return to the creation of the recombinant viruses that seeded the pandemic. I believe it is extremely hard to imagine that if all this rampant viral diversification, and then recombination, had been going in Leo between the 1930s and 1970s, as Hahn proposes, that none of these viruses managed to escape from Leo until the 1970s. (After all, it is not only in Leopoldville that people had sex in those decades.)

By comparison, these very same conditions (the emergence of several subtypes, and rampant recombination between the subtypes) represent no problem at all to the OPV theory. Indeed, it is exactly what the theory predicts.

First of all you need many different strains of immunodeficiency virus (whether in humans or chimps) coming into contact with each other in the same place. Hahn argues that this happens in Leo, after just one single human infected with chimp SIV arrives in that city (from Cameroon or Congo Brazzaville), and the virus diversifies from there.

But where better for such a thing to have happened than in the largest chimpanzee colony the world had ever seen up to that point – at Lindi camp, just outside Stanleyville, which, in the course of three and a half years, housed more than 500 chimps and bonobos from a wide range of different localities?

Courtesy of the work of Dr Hahn and Sharp, it seems that between 10% and 13% of Pan troglodytes troglodytes chimps and approximately 20% of Pan troglodytes schweinfurthii chimps[17] are likely to be naturally SIV-infected in the wild. Since most of the 400-odd chimps and bonobos that were directly involved in the polio research at Lindi and the LMS are known to have been Pts chimps, it is likely that between 60 and 80 of these animals would have been naturally infected with SIV on arrival at the camp. Because the chimps came from different venues spread across at least 200,000 square miles of rain forest, these SIVs must have included some widely differing strains, including, it now seems probable, some Pan troglodytes troglodytes strains. Indeed, as I have proposed in my italicised section above, these may have included some of those Ptt SIV strains from south-eastern Cameroon that Hahn thinks are the very closest relatives to pandemic HIV-1.

My belief, however, is that for the OPV scenario to work, it is not requisite that any of the Cameroonian Ptt SIVs, or indeed any Ptt SIVs at all, were present at Lindi camp or at the LMS. The Pan troglodytes schweinfurthii (Pts) chimps found all around Stanleyville on the north bank of the Congo have their own SIV strains, and these strains have exactly the same nine genes that also appear in the Ptt SIVs and in pandemic HIV-1. It’s simply that the OPV hypothesis works even better if there were also some Ptt chimps in Stanleyville or at Lindi. And we now know that there was at least one of them present.

Back to recombination. First of all, these differing strains of SIV would have started recombining in the cages, and in the group-cage, at Lindi camp, where chimps from different places met – and often fought. (Fighting is now recognised as the prime mode of onward SIV transmission between different primates.)

But in this scenario, how do the chimp SIVs get to infect humans? For various reasons I do not want to reprise all the evidence now, but some of it has already appeared on this web-site, and some other parts appear in the documentary film, "The Origins of AIDS".[6]

However, let me summarise. We now know from several different witnesses from Lindi camp that the LMS doctors were routinely harvesting blood and organs, including kidneys, from the Lindi chimps. Furthermore, they were regularly draining the chimps of much of their blood on the day before they were sacrificed. Sometimes as many as four or five animals were "sacrificed", as they put it, on a single day. We know from LMS employees (including the Belgian head technician of the lab) that they were making chimp tissue culture "for a long time" at the LMS, and that this tissue culture was being supplied to the head of virology, Paul Osterrieth, who was (although he denies it) in charge of the polio vaccines. Osterrieth was also, according to the witnesses in his own laboratory, in charge of preparing further batches of the polio vaccine (in other words, growing them in the chimpanzee tissue cultures). We also know from documentary evidence that a procedure used by the LMS researchers to keep their chimp cells alive involved using "isologous sera" (the sera of other chimpanzees) as a growth and maintenance medium. (This alone would have provided materials from at least two different chimps in a culture, which allows the theoretical possibility of SIV recombination. However, such sera would almost certainly have contained pooled material from several different animals, which provides an even better opportunity for in vitro recombination between different SIV strains).

A retrovirologist with considerable experience in this field has informed me that the presence in a tissue culture of cells from chimpanzees coming from two different species or subspecies, or even from two different troops would by itself be sufficient to activate the T-cells in that culture, and therefore to allow SIV growth, replication – and recombination. (This is because different chimp troops would almost inevitably contain animals that were not matched immunologically, with respect to MHC, or major histocompatability complex. In other words, HIV or SIV growth in vitro does not require the addition of a special agent such as "T-cell growth factor", which Robert Gallo used to grow HIV-1 in vitro in the 1980s, and which, some have argued, would have been required as an ingredient in the Stanleyville tissue cultures for the OPV/AIDS theory to remain viable. In reality, all it would require would be the addition of SIV-infected cells or sera from chimps coming from two different parts of the rain forest.) Furthermore, since, as Robin Weiss himself has reported, all early tissue cultures contained a small percentage of macrophages, it is likely that the SIVs therein would have prospered anyway, which renders the question of MHC haplotype irrelevant.

The major point is that chimpanzee SIVs would have replicated and recombined in such a tissue culture, and that a proportion of SIV virions (how big a proportion would depend on the specific preparation techniques used for each tissue culture and vaccine batch) would be expected to survive through to the final vaccine. Since Dr Osterrieth is in denial about all this [see below], it is impossible to know exactly how the Stanleyville vaccine batches were prepared, and impossible to do a trial run to test how much SIV in such batches might have survived. But the virological message is this. If the Stanleyville vaccine was indeed prepared in chimp cells and chimp sera, there is no reason to suppose that SIVs, including recombined SIVs, would not have survived through to the final vaccine that was given to humans.

As reported above, there is eye-witness evidence confirming every step of the process whereby tissue cultures were prepared from the Lindi/Stanleyville chimps. But most crucially of all, there are three witnesses who were directly involved with the chimpanzee experiments (two Belgians and an American) who confirm that the LMS doctors were indeed making polio vaccines locally in the Belgian Congo, using cultures from the Stanleyville chimpanzees. Others who were only indirectly involved have confirmed this.

Dr Osterrieth, by contrast, claims that he couldn’t possibly have prepared polio vaccine in the Stanleyville laboratory: that they didn’t have the means or equipment to do this. But that is patent nonsense.

Provided glassware is kept clean and the work is done in sterile conditions, making vaccine batches of polio vaccine is not – and was not – a difficult procedure.

Indeed, during 1957 Osterrieth was being trained in these very techniques by Koprowski’s assistant, Tom Norton, in the labs at the Wistar Institute in Philadelphia. Furthermore, by the time he returned from the US, Osterrieth was working in the virology lab of the new LMS building which opened in September 1957. It was a brand-new custom-built lab, 100 metres long and two storeys high, and funded (it seems) by mysterious sources (for the Congolese government had no spare cash for such indulgences).

And there is more. Between 1953 and 1957, a Polish vet, Alexandre Jezierski, working in his small veterinary lab at Gabu in eastern Belgian Congo, did exactly what Osterreith claims was "impossible" to do in Stanleyville. Without very much fuss, Jezierski prepared tissue cultures from the cells of fifteen different African primate species, including the chimpanzee. He then went on to prepare polio vaccines (both inactivated and oral) in at least five of these primate tissue cultures.

The only difference was that Jezierski’s locally-made vaccines were given to only 21 African "volunteers". As it turns out, the OPVs he gave them were not dangerous, having (by good fortune) been grown in colobus cultures.

By contrast, the batches of CHAT polio vaccine that were locally-prepared at the LMS were given to up to one million Africans in 31 known vaccination venues spread around the Belgian Congo, Rwanda and Burundi. Including, of course, Leopoldville, where every African child up to the age of five was vaccinated, a total of 76,000 kids.

The correlations between the 31 different CHAT vaccination venues and the places where HIV-1 first emerged in Africa (all of which are found in villages and towns in the DRC, Rwanda and Burundi) are "highly significant". That means there is less than a 1 in 1,000 chance that these correlations are caused by coincidence alone.

Given the foregoing, it seems highly probable that many or all of the vaccine batches that were locally-prepared in Stanleyville would have contained not just attenuated poliovirus, but also a range of recombinant and mosaic versions of various strains of chimp SIV.

As a result, chimp SIV strains, including recombinant strains, would have been spawned right across the vaccinated towns and villages of the DRC, Rwanda and Burundi….including, of course, in Leopoldville.

But the recombination factor does not end there, for once chimp SIV strains had been seeded in different groups of vaccinees, further in vivo recombination would have occurred through the more traditional means of people having sex with each other. Indeed, it is even possible that some of the CHAT vaccinees were people (perhaps bushmeat-sellers or chimp-hunters) who had previously been exposed to Pts or Ptt SIV through bushmeat. If they were, then transient infection with just a single SIV strain via the bushmeat would very probably not have caused any illness. But what if a chimp SIV strain from the polio vaccine and a strain of chimp SIV acquired from bushmeat recombined in vivo, in the body of an infected chimp-hunter somewhere in the Belgian territories of Africa?

What did Tom Folks’s group write? "We propose….that some recombinant viruses most likely seeded the early global epidemic."

The events at Lindi camp, where almost 400 chimps were sacrificed for (largely undocumented) poliomyelitis research during the course of two terrible years, and the creation at the LMS of living oral polio vaccines that were prepared in the cells and sera of these same chimps, surely provides the recombination factors that are so clearly missing from Beatrice Hahn’s scenario.

After sixteen years of historical and scientific research into the origins of AIDS, I feel very confident that this is how the AIDS pandemic started.

A Single or Multiple Source?

There is one other key detail to deal with. Hahn and Co. insist that the pandemic began with a single chimp virus infecting a human.

I disagree. I believe that it began after several different variants of chimp SIV (almost certainly of recombined chimp SIVs) transferred to humans at almost the same point in time (ie within the course of approximately three years), via the different batches and trials of locally-prepared CHAT oral polio vaccine.

The geneticists’ methods of modelling do not postulate such a scenario; in other words, they automatically reject it. That doesn’t make it wrong, however. On the contrary, their failure to consider this possibility reflects only the limitations of their thinking, and of their methodology.


Dr Hahn’s new Pan troglodytes troglodytes chimpanzee SIVs from Cameroon are genetically closer to pandemic HIV-1 than any other primate SIVs previously reported.

However, they hardly represent the "cradle" of pandemic HIV-1, or "dead ringers" for the AIDS virus, as she and her group would have us believe.[3]

A far likelier explanation for bridging the genetic gap between the viruses is recombination in vivo among the collectively-caged chimpanzees of Lindi camp, and recombination in vitro, in Stanleyville, Belgian Congo, between chimp SIVs (very probably including Pan troglodytes troglodytes SIVs) that were growing unseen and unrecognised in tissue cultures that were prepared at the LMS from chimpanzee cells and sera. These same chimpanzee tissue cultures were used in the LMS virology department to prepare locally-made batches of CHAT oral polio vaccine, that were then administered to up to one million African "volunteers" in 31 known central African trials.[6] [12]

These OPV trial venues are the places where pandemic HIV-1 and AIDS first emerged in the world – and they are hundreds of miles away from the chimps of south-eastern Cameroon favoured by Beatrice Hahn.

I believe that this is a far likelier explanation for how AIDS began than the arguments so dogmatically advanced by the key proponents of the bushmeat hypothesis.

Ed Hooper. 16/06/06, updated 5/08/06.


[1] B.F. Keele, B.H. Hahn et al., "Chimpanzee Reservoirs of Pandemic and Nonpandemic HIV-1", [Science Express: 10.1126/science.1126531, and Science, 2006; 313; 523-526.].

[2] P. M. Sharp, "Where AIDS Came From" [Webcast]; 13th Conference on Retroviruses and Opportunistic Infections; Denver, CO, February 5-8, 2006.

[3] F. Deinhardt, Lindi Databook, 1959.

[4] M.M. Vastesaeger et al.; "L’atherosclerose experimentale du chimpanze. Recherches preliminaires"; Acta Cardiol.; 1965; Supp. 11; 283-297.

[5] "The Age of AIDS", PBS documentary, 2006. M. Carmichael, "How it began: HIV before the age of AIDS"; article available on PBS web-site, at: http://www.pbs.org/wgbh/pages/frontline/aids/virus/origins.html.

[6] "The Origins of AIDS"; MFP/Galafim documentary, 2004.

[7] A. Andre, G. Courtois. G. Ninane, P.M. Osterrieth et al.; "Mise en evidence d’antigenes de groupes sanguins A, B, O et Rh chez les singes chimpanzes"; Ann. Inst. Past.; 1961; 101; 82-95.

[8] M. L. Kalish, T. M. Folks et al.; "Recombinant Viruses and Early Global HIV-1 Epidemic"; Emerg. Inf. Dis.; 2004; 10; 1227-1234.

[9] The remaining HIV-prevalence data for CAR, Cameroon and Congo (Brazzaville) were obtained from the HIV/AIDS Surveillance Database; International Programs Center, US Bureau of the Census; January 1997 edition.

[10] National Public Radio, "Weekend Edition", broadcast June 4, 2006, 12:00 PM EST. Transcript, with headline: "Origin of AIDS Linked to Colonial Practices in Africa."

[11] F. van Heuverswyn, "Natural Reservoirs of Chimpanzee Lentiviruses Closely Related to HIV-1 Groups M and N" [Webcast]; 13th Conference on Retroviruses and Opportunistic Infections; Denver, CO, February 5-8, 2006.

[12] E. Hooper, "Dephlogistication, Imperial Display, Apes, Angels, and the Return of Monsieur Emile Zola. New developments in the origins of AIDS controversy, including some observations about ways in which the scientific establishment may seek to limit open debate and flow of information on ‘difficult’ issues"; Atti dei Convegni Lincei; 2003; 187; 27-230.

[13] G. Courtois, "Sur la réalisation d’une singerie de chimpanzés au Congo"; Proceedings of Symposium international sur l’avenir des animaux de laboratoire; Lyon 1966, 235-244; (Institut Merieux, Lyon: 1967).

[14] J. Kingdon, The Kingdon Field Guide to African Mammals; (Academic Press, San Diego: 1997), p. 10.

[15] "P. Gagneux, P.A. Morin et al., "Gene flow in wild chimpanzee populations: what genetic data tell us about chimpanzee movement over space and time", Phil. Trans. Roy. Soc. Lond. B; 2001; 356; 889-897.

[16] M. Worobey, B. Hahn et al., "Contaminated polio vaccine theory refuted" [letter]; Nature; 2004; 428; 820.]

[17] P.M. Sharp, G.M. Shaw and B.H. Hahn, "Simian Immunodeficiency Virus Infection of Chimpanzees"; J. Virol.; 2005; 79(7); 3891-3902.

The Emperor’s New Clothes: Beatrice Hahn and The Latest Mumbo Jumbo

Sadly, some scientists seem to believe that by repeating an untruth often enough, you can persuade the world that it is actually true.

One such group of scientists is that led by Dr Beatrice Hahn of the University of Alabama, whose members seem to be much more interested in trying to earn themselves grants and glittering prizes than in actually helping us understand how the AIDS pandemic began.
Continue reading “The Emperor’s New Clothes: Beatrice Hahn and The Latest Mumbo Jumbo”

The Bushmeat Theorists Fail to Deliver Once Again


The following article was originally written in December 2005, and represents the draft of a letter which I had intended to send to Emerging Infectious Diseases in response to an article published in that month’s issue of the journal by a team led by doctors Nathan Wolfe and Donald Burke from Johns Hopkins University in Baltimore, Maryland, USA.
The title of the article, "Central African hunters exposed to simian immunodeficiency virus", is amusing, because what Wolfe and Burke actually demonstrate in their article is the exact opposite. Not one of the African hunters whom they tested showed any evidence of SIV exposure.

Just one of more than a thousand members of the general Cameroonian population showed some signs (by a single assay, ELISPOT) of exposure to an SIV from a colobus monkey. However, other HIV/SIV antibody assays conducted on this sample were negative, and when the researchers tried to confirm that they had found a true SIV, using PCR (polymerase chain reaction) techniques, they came up negative. There is therefore a real possibility that their one apparently positive result was actually a false positive. Even if it were a genuine positive, it would offer only very limited support to the bushmeat theory of origin of AIDS.

Doctors Wolfe and Burke and their co-authors are to be congratulated for publishing their predominantly negative findings, even if they are not to be congratulated for publishing such findings under a gratuitously misleading title!

A more appropriate title for this article might have been "Failure to detect SIV transmission from local primates to Cameroonian bushmeat hunters".

My letter of response to Emerging Infectious Diseases was never submitted, largely because its length exceeds the journal’s guidelines for readers’ letters. I have decided instead to make minor emendations, and to post it on this web-site.

Ed Hooper. 28/3/06

Dear Sir,

Meaningful research into simian immunodeficiency virus (SIV) infections in African primates, and into potential future zoonoses, is to be welcomed, and in many respects doctors Wolfe and Burke and their collaborators are to be commended for their ongoing efforts in this area. However, it is concerning that recent articles by these authors display a disparity between the very significant data that have been collected and the conclusions derived therefrom.

One of the earlier articles by these authors (1) was entitled "Naturally acquired simian retrovirus infections in central African hunters", and reported significant levels (10 of 1,099 = 1%) of simian foamy virus (SFV) infection among Cameroonians from nine villages sited close to natural non-human primate habitats who reported direct contact with the blood or body fluids of wild non-human primates, "mainly through hunting and butchering". The article theorised that SIVs could also be transmitted to humans in this way, but it did not report the detection of any human infections with SIVs. Subsequent enquiries about this topic to Dr Wolfe merely elicited the response that research was ongoing.

Wolfe and Burke’s latest article is entitled "Central African hunters exposed to simian immunodeficiency virus" (2), but it documents the exact opposite. Just one of 1,224 Cameroonian plasma tested showed some indications of exposure to an SIV (in this case SIVcol, from Colobus guereza) by ELISPOT assay, but the plasma in question did not come from any of the "hunters", namely the 76 persons tested who reported high levels of exposure to the bodily fluids of non-human primates (NHPs) by hunting, butchery or pet-keeping. Instead, it came from one of the 1,071 members of "a general population of urban and rural areas of Cameroon, where people may handle NHP meat but are unlikely to have repeated contact with the blood or body fluids of freshly killed animals".

The ELISPOT-positive plasma showed strong humoral, but only weak cellular immune reactivity to SIVcol peptides, and the authors were unable to amplify any SIV nucleic acids by PCR. The authors proposed that this could be indicative of a virus hiding in lymphatic tissues, but a likelier explanation is that this was a false positive, or that the one human exposure to SIV that they had detected had failed to cause productive infection.

In an accompanying "Perspective" piece (3), the same authors list "some zoonotic pathogens that have emerged in the Cameroon-Congo Basin Region, 1970-2005". Nine of the ten pathogens listed are identified as causing only limited human exposure, either without replication, as single infections, or as localised outbreaks or epidemics. The tenth pathogen is HIV, and it is proposed that this arose among hunters and butchers when SIV was transmitted via "repeated single infections or localised outbreaks, followed by national then global emergence". But the first crucial step of this transmission chain (the productive SIV infection of local hunters or butchers) is precisely what the authors have thus far failed to establish. In short, Wolfe and Burke are jumping the gun, for although their data suggests that Africans may perhaps be occasionally exposed to SIVs through cutting up bushmeat, they have as yet provided no evidence that such SIVs either replicate in humans, or cause productive infections.

Few would deny the theoretical possibilities that human exposures to SIVs through bushmeat might sometimes occur, or even that such exposures might sometimes cause productive infections. What is at issue is whether such human infections with SIV (if indeed they occur), are likely to have sparked either epidemic outbreaks, or the AIDS pandemic.

There are indeed ten known examples of HIVs that seem to have derived from distinct zoonoses (HIV-1 Groups M, O and N, and HIV-2 Groups A to G, inclusive), but it seems that only five of these (HIV-1 Groups M, O and N, and HIV-2 Groups A and B) have sparked either outbreaks or epidemics, and all five of these outbreaks appear to have occurred in or around [or perhaps in the case of HIV-1(N) shortly after], the 1950s. This factor alone (the lack of evidence of any HIV infections prior to the 1950s) suggests that the hand of modern man, or, more specifically, the hand of modern medical man (ie iatrogenic factors), may have played a key role.

The most ironic aspect of this is that while advocates of the bushmeat origin of HIV seem once again to be making premature claims, another far more precisely documented theory of HIV origin, the oral polio vaccine (OPV) theory, has been repeatedly (and wrongly) described in scientific journals as "destroyed" or "refuted". Yet all five of the recognised HIV outbreaks coincide with areas where experimental polio vaccines produced in African primate cells are known (or believed) to have been administered to large populations of Africans in the late 1950s. [4] By contrast, there is only a tenuous epidemiological linkage between the hearth of HIV-1 as mooted by proponents of the bushmeat theory (which according to their latest version of events, lies in or very near south-eastern Cameroon), and the observed epicentre of pandemic (HIV-1 Group M-related) AIDS in the Democratic Republic of Congo (DRC, former Belgian Congo), Rwanda and Burundi.

Furthermore, there is to date no evidence of HIV-1(M) infection in the Cameroon/Gabon/Congo Brazzaville region to the north of the River Congo before the year 1981. This is more than 20 years after the first evidence of HIV-1(M) in Leopoldville/Kinshasa [DRC], five years after the first evidence of HIV-1(M) in Yambuku and Abumombazi (northern DRC), four years after the first evidence of the virus in Kigali, Rwanda, and a year after the first evidence of the virus in Bujumbura, Burundi.

During the 1950s, the approved standardisation procedures for polio vaccines allowed for them to be cultivated in the cells of any viable primate, and although most such vaccines were prepared in the cells of Asian monkeys such as the rhesus and cynomolgus macaques, vaccines prepared in the cells of several species of African primates were also used in a surprisingly large number of human trials. As we now know, several of these African primate species are host to their own SIVs.

Let me give just one example. From 1955 onwards the ancestral host to HIV-2, the sooty mangabey, Cercocebus atys, was one of many primates that were used for polio vaccine testing and propagation. The Pasteur Institute vaccine that was used in Europe was an inactivated polio vaccine (IPV), and was prepared mainly from the cells of Papio papio, the Guinea baboon, originating from West Africa. Large numbers of baboons were captured and held in collective pens at the Institut Pasteur facility at Pastoria, near Kindia in present-day Guinea Conakry. However, other "small monkeys" were also held in these same pens, and these included sooty mangabeys. A Guinean scientist who worked at Pastoria in the 1950s and who directed the facility from 1961 onwards has informed me that starting in 1956, Pasteur-produced polio vaccines were administered on a large scale by injection in French West Africa. (From 1955 to 1958, the Pasteur Institute’s director of virology, Pierre Lepine, wrote several articles about the comparative benefits of killed and live polio vaccines, in the course of which he discussed the possibility of administering a third dose of attenuated vaccine, after establishing immunity with two prior injections of inactivated vaccine. He indicated that he and his colleagues had "conducted experiments along these lines, and we continue them, but we can only proceed with very great prudence and much deliberation.") One of the ways that Lepine proposed administering this live vaccine dose was, rather surprisingly, by injection, rather than by mouth. According to the Guinean scientist, this regime of injecting two doses of inactivated polio vaccine followed by one injection of live polio vaccine was indeed employed in French West Africa shortly after 1956.[4]

Apart from man and the sooty mangabey, it seems that the only other African primate that can be persistently infected with HIV-2-like viruses is the baboon. [5] There are therefore two potential ways in which vaccine stock used in Africa in the 1950s could have become infected with the HIV-2 precursor. A batch or batches could have been prepared direct from the cells of an SIV-infected sooty mangabey, or a batch or batches could have been prepared from baboons that had been co-caged with sooty mangabeys, and infected with SIV from the latter species via bites or scratches.

There are strong indications that the Portuguese also administered polio vaccines in their overseas territories, including Portuguese Guinea, now Guinea-Bissau, during this period. There is no record of the Portuguese having developed their own vaccine during the 1950s, but they may have used vaccine batches prepared either at the Pasteur Institute in Paris or at one of the Pasteur branches in Dakar (Senegal) or Pastoria, for during that era Pasteur scientists shared several other locally-prepared vaccines with the contiguous territory of Portuguese Guinea. [4] The earliest known appearance of HIV-2 in humans was in 1965, and West Africa (and in particular Guinea-Bissau) represents the hearth of the known HIV-2 outbreaks.[6]

Similarly the ancestral host of HIV-1, the common chimpanzee, Pan troglodytes, was among the primates that were collected in large numbers at both Franceville and at Gamaba farm (near Brazzaville), in French Equatorial Africa, in the second half of the 1950s. It is reported that cells from primates at Gamaba were used to "grow poliovirus" in the Pasteur Institute lab in Brazzaville from 1957 onwards, at a time when scientists based at that lab was conducting human trials of both IPV and OPV in French Equatorial Africa. At least one of the trials of an injected vaccine took place in 1957 at Mitzic (in the north of present-day Gabon) and in the eastern part of the contiguous territory of Spanish Guinea (now Equatorial Guinea), in an area which lies adjacent to the mooted hearths of the "minor variants of HIV-1", Groups O and N, in southern Cameroon. The earliest known infectee with HIV-1 Group O, a Norwegian sailor, appears to have become infected during a trip to Yaounde, Cameroon, in the winter of 1961-2 [7]. HIV-1 Group N was first detected in Cameroon in 1995, and the leading researcher into Group N, Francois Simon, writes that the virus may have emerged in humans some time between about 1970 and 1975, "though", he adds, "this is purely speculative".[8].

A far larger chimpanzee collection scheme based at the Laboratoire Medical de Stanleyville, in the Belgian Congo, was in operation from 1956 to 1960, and by 1958 "some 400" chimpanzees had been collected at an isolated nearby facility, Lindi camp, for the purpose of "perfecting" or "putting the finishing touches to" CHAT, an OPV developed by the Polish-American scientist, Hilary Koprowski. Officially, these chimps were merely used to "test" (ie evaluate the safety and efficacy of) Koprowski’s experimental oral polio vaccines. However, personal testimonies from several Belgian and Congolese scientists and technicians, and two Belgian medical administrators, reveal that cells from the Lindi chimps were used to make tissue culture in the Stanleyville lab, and that this tissue culture was then used to prepare batches of locally-made polio vaccine. This locally-made vaccine (together with vaccine prepared in the USA) was administered in mass trials in the Belgian Congo and Ruanda-Urundi from mid-1957 (at latest) until August 1959, when CHAT vaccine was officially approved by the Belgian Congo authorities for feeding to all ages and races upon request. (Various lines of research suggest that from that month onwards, only fully safety-tested vaccine was used, in preference to locally-made batches.) In these former Belgian territories, there is a highly significant correlation between the places where this OPV (CHAT) was fed, and the first appearances of HIV-1 Group M, and of pandemic AIDS. The first evidence of HIV-1 Group M virus comes from a blood sample obtained from a male subject in Leopoldville (Kinshasa), allegedly in 1959, although the precise history of this blood sample is unclear, and it may in reality have been drawn between one to four years later. The age of the male subject is also unknown and, in contrast to previous reports, it is quite possible that he was a child at the time that his blood was tested. If so, then he would presumably have also been a CHAT vaccinee, for all Leopoldville children aged up to five years were vaccinated with CHAT between August 1958 and Aoril 1960. The earliest death from Group M-related AIDS seems to have occurred in 1962 [9].

Since the emergence of the OPV/AIDS theory, the great majority of the persons involved with these polio vaccine trials energetically deny that they ever prepared human polio vaccines from local primate tissues, but their accounts are characterised by internal contradictions and provable errors.[10] Moreover, their versions of events are contradicted by an ever-increasing number of witnesses to, and participants in, these events. However, the CHAT vaccine-makers have been supported by many present-day virologists and public health officials, even if these individuals do not have first-hand experience of the vaccine trials. Many of these individuals, however, have research interests and public health preoccupations which coincide rather closely with the disproving of the controversial or "ugly" theory of OPV/AIDS.[11] They apparently fear that if the AIDS pandemic should ever come to be directly linked to inappropriate medical experimentation, then popular faith in public health initiatives, such as vaccination campaigns, may be irrevocably shaken.

Several alleged "refutations" of the OPV theory of AIDS origin have been broadcast in science magazines and in the medical literature, but none of these refutations have been supported by any hard data. The most popular "refutations" are the following: (a) that batches of CHAT have been tested, and found to be free of HIV, SIV and chimpanzee DNA; (b) that phylogenetic dating analysis proves that the most recent common ancestor (MRCA) of HIV-1 existed in or around 1931, twenty or more years before the OPV trials, and (c) that the subspecies of chimpanzee held at Lindi camp was different from the subspecies of the mooted HIV-1 precursor host, Pan troglodytes troglodytes.

Yet on closer examination, none of these arguments hold water.

(a) The CHAT vaccine samples that were belatedly released for molecular analysis were all produced or prepared in the USA, whereas the vaccine batches that need to be released (if they still exist) and tested are those that were prepared in Africa, for instance in Stanleyville.
(b) Phylogenetic dating analysis is an inappropriate technique for measuring the evolution of a lentiretrovirus such as HIV: it measures only evolution by mutation, whereas 90% of the evolution of the HIVs occurs through recombination. Such attempts to date HIV by a molecular clock are innately bogus.
(c) The chimps at Lindi did not merely originate from "the vicinity of Stanleyville", but came from an area of 300,000 square miles of rain forest, including regions such as the Congo river below Mbandaka, where Pan troglodytes troglodytes chimps are among those that are bought and sold, and transported up-river. In short, the Lindi chimps (which were both co-caged and group-caged) are likely to have included a number of animals infected with one or more variants of "the HIV-1 precursor virus". The situation is further complicated by the chimpanzee tissue cultures that were prepared in the Stanleyville lab, which apparently used pooled chimpanzee sera as growth or maintenance medium. The Lindi camp/Laboratoire Medical de Stanleyville research thus offered multiple opportunities for recombination between different chimp SIVs, and their later dissemination into various African populations where CHAT vaccine batches were tested.[12]


It is now nearly fourteen years since Beatrice Hahn and Paul Sharp published an article entitled: "Human infection by genetically diverse SIVsm-related HIV-2 in west Africa" [13], which provided persuasive evidence that an HIV-2 infection had been acquired by a Liberian man from a sooty mangabey (while leaving open the route of cross-species transmission). For fourteen years researchers (including Hahn, Sharp, Burke and Wolfe) have been searching feverishly for similar evidence of human infection with chimpanzee SIV-related HIV-1 Group M among west central African hunters – and failing to find any such evidence. This latest article – and its deliberately misleading title – only serves to emphasise the weakness of their position.

They know what they want to find, and they are desperate to find it, come what may. Perhaps the reason why they keep failing to deliver is that their "certainties" are not certainties at all. Their long-term refusal to even countenance the OPV/AIDS hypothesis suggests that they may be in denial, and more afraid of the hypothesis than they care to admit.

Doctors Burke and Wolfe are not alone in their assumption that the AIDS pandemic virus, HIV-1 Group M, must have evolved through human contact with chimpanzee bushmeat, but their conclusions are, to say the least, premature. Any sincere approach to unravelling the origins of the HIVs must continue to examine the history of the experimental polio vaccines that were administered in the Belgian Congo, and elsewhere in sub-Saharan Africa, during the second half of the 1950s.

Edward Hooper. 28/3/06.


(1) Wolfe ND, Folks TM, Burke DS et al, "Naturally acquired simian retrovirus infections in central African hunters"; Lancet; 2004; 363; 932-937.

(2) Kalish ML, Wolfe ND, Burke DS, Folks TM et al.; "Central African hunters exposed to simian immunodeficiency virus"; Emerging Infectious Diseases; 2005; 11(12); 1928-1930.

(3) Wolfe ND, Burke DS et al.; "Bushmeat hunting, deforestation and prediction of zoonoses emergence"; Emerging Infectious Diseases; 2005; 11(12); 1822-1827.

(4) Hooper E, "The River", E. Hooper, [Boston: Little, Brown and Co, 2000 (paperback edition)]; 827-877, but especially 831-834. [Note that in the paperback edition these pages represent a completely rewritten postscript. In the Penguin UK (paperback) edition, this new postscript featured on pages 827-874, with the highlighted passage on 831-833.]

(5) Castro BA, Levy JA et al.; "Persistent infection of baboons and rhesus monkeys with different strains of HIV-2", Virology; 1991; 184; 219-226.

(6) Hooper E, "The River", [Boston: Little, Brown and Co, and London: Penguin, 2000], pages 623-643.

(?) Sharp speech

(7) Hooper E, "Sailors and starbursts, and the arrival of HIV"; British Medical Journal; 1997; 315; 1689-1691.

(8) Simon F, personal communication, March 2000.

(9) Hooper E, "The River", 259-262.

(10) Plotkin SA, "Untruths and Consequences"; Phil Trans. R. Soc. Lond. B; 2001; 356; 815-823. Plotkin SA et al., "Postscript relating to new allegations made by Edward Hooper at the Royal Society Discussion Meeting on 11 September 2000", Phil Trans. R. Soc. Lond. B; 2001; 356; 825-829. Koprowski H, "Hypotheses and Facts"; Phil Trans. R. Soc. Lond. B; 2001; 356; 831-833. Osterrieth P, "Vaccine could not have been prepared in Stanleyville", Phil Trans. R. Soc. Lond. B; 2001; 356; 839. [See also other articles by these authors, together with E. Hooper’s commentaries on same, all available on this web-site.]

(11) Weiss RA, "Polio vaccines exonerated"; Nature; 2000; 416; 1035-1036.

(12) Hooper E., "Dephlogistication, imperial display, apes, angels and the return of Monsieur Emile Zola. New developments in the origins of AIDS controversy, including some observations about ways in which the scientific establishment may seek to limit open debate and flow of information on ‘difficult’ issues"; Atti dei Convegni Lincei; 2003; 187; 27-230.

(13) Gao F, Sharp PM, Hahn BH et al., "Human infection by genetically diverse SIVsm-related HIV-2 in west Africa"; Nature; 1992; 358; 495-499.