The Story of a Man-Made Disease

17 March, 2003; revised 22 April, 2003.

A much abbreviated and modified version of this article appeared as “Aids and the polio vaccine”, London Review of Books, Vol. 25, No. 7, 3 April 2003,

When their leaders cannot be relied upon, people believe what they are led to believe. Truth and knowledge become perverted by political expediency, by the needs of the day.

How does one persuade trusting citizens that an emperor is naked? In the fairy story, it takes the naïve candour of the little boy who is too young to realise the consequences of speaking out of turn. But once he does speak, the rest of the people look up and see that what he says is true, that their ruler is behaving with an imperial disregard for both truth and decency.

Let us see if that works in the real world, too.

Gentlemen and ladies, people of the town. I wish to make an announcement.

AIDS is a man-made disease.

It is now all but certain that it was human hands (and, in particular, those of the doctor and the scientist) that started the AIDS pandemic, which now represents the worst outbreak of infectious disease the world has ever seen.

27 million deaths. More than 66 million infected with HIV since the pandemic began. No wonder everyone insists that the emperor is draped in finery.

I have spent the last seventeen years working on AIDS, and the last thirteen investigating its origins. During that time I have had help and sometimes tuition from the brightest and the best, which includes not only scientists and historians, but also some of those who played a crucial role in the events detailed below. During the first two years of the nineties I looked at more than a dozen theories about how AIDS began, most of which could be disposed of by a few hours or days of research. I first came across the oral polio vaccine (OPV) theory in 1992, and found that it could not be readily dismissed. A year later I began working with Bill Hamilton, the great evolutionary biologist, who was himself already intrigued by the theory and who soon became its most eminent scientific supporter. In 1999 my book about the OPV theory, The River: A Journey to the Source of HIV and AIDS, was published, and it sparked a controversy which in turn led to the staging of two conferences on the origins of HIV and AIDS, held at the leading institutes of scientific research in the UK and Italy: the Royal Society in London, and the Accademia dei Lincei in Rome.

Bill Hamilton was the originator and co-organiser of the Royal Society meeting, but his participation was prevented by his untimely death in March 2000, which followed his second expedition to the Congo to seek data relevant to the hypothesis. The two surviving organisers, Robin Weiss and Simon Wain-Hobson, went ahead with the conference, but there were small and subtle changes. It was as if the grandees of Science had got together to protect their own, and they did so rather well. The schedule and running order were adjusted here and there, test results of dubious relevance were presented as if they represented compelling evidence, and Professor Weiss made a closing speech which came down heavily against the theory. (At the time, he admitted that his conclusions might be “biased … my plain personal prejudice”, but this passage did not appear in the published version of his speech.) The Rome conference a year later (of which the proceedings have just been published) was much more balanced, but again Weiss came along to deliver the closing summary, and to damn the theory once more.

The OPV theory requires a little background. In the fifties, oral polio vaccines (which are living vaccines, in contrast to the injected variety, IPVs) were prepared in primate cells. (In fact, most still are today.) Thus each OPV contained not only live, weakened poliovirus, but also whichever monkey viruses happened to be present in the cells used to grow the vaccine. One such virus was SV-40 (the fortieth simian virus to be discovered), which was found in 1960 to cause tumours in hamsters. By then, tens of millions around the world had been given SV-40-contaminated polio vaccines, and over the next two years, polio vaccine producers switched from using Asian monkeys (many of which are infected with SV-40) to African monkeys (which are not). Forty years on, many scientists acknowledge that exposure to SV-40 leads to a slightly heightened risk for certain cancers such as mesothelioma.

The OPV theory, by contrast, relates to a very different polio vaccine. It proposes that an experimental OPV called CHAT, developed at the Wistar Institute in Philadelphia by a Polish-born American virologist, Hilary Koprowski, sparked the AIDS pandemic by introducing the simian immunodeficiency virus (SIV) of the common chimpanzee into some of the roughly one million Africans who were fed the vaccine between 1957 and 1960. Chimpanzee SIV is now widely recognised as the direct ancestor of the pandemic strain of HIV (HIV-1 Group M), which has caused approximately 99% of the world’s 66 million HIV infections. In Africa, CHAT vaccine was fed only in Belgian-ruled territories: in the Belgian Congo (nowadays the Democratic Republic of Congo, DRC) and the former UN trusteeship of Ruanda-Urundi (nowadays Rwanda and Burundi). These are also the countries that represent the epicentre of the AIDS pandemic. The Laboratoire Médical de Stanleyville (LMS), which tested CHAT vaccine for safety and coordinated the early African vaccinations, was situated just a few miles from a chimpanzee colony, Lindi camp, which operated from 1956-1960. During those years, more than 500 chimps and pygmy chimps (bonobos) were sacrificed there, mostly in the course of the polio vaccine research. Almost complete secrecy surrounded that research. The only official statements about Lindi camp were brief and anodyne.

In contrast to the OPV theory, the theory of origin favoured by most in the medical establishment is usually called the cut hunter, or natural transfer theory. This proposes that a single hunter or bushmeat seller became infected with chimp SIV while skinning or butchering a chimp, and that the AIDS pandemic started from that single infection. The theory is more nebulous, and thus more difficult to prove – or disprove.

Before the Royal Society conference in September 2000, half a dozen samples of CHAT vaccine had been selected from the freezers at the Wistar Institute, and then independently tested in three separate labs. (The Wistar had promised to allow this testing back in 1992, but then nothing further happened.) The results were announced at the meeting: no trace of HIV, SIV, or chimpanzee DNA, was found. A press conference had been scheduled to follow this announcement, and much was made of the negative findings. Rather surprisingly, given the mode of selection of the samples, and the fact that none had specifically been prepared for the 1950s African trials, the results were widely taken by medical journals, and by the popular press, to constitute a concrete disproof of the OPV theory.

There were several aspects of the Royal Society meeting that troubled me deeply. One was that the playing-field had not been level: for instance, a clear majority of speakers came from the anti-OPV camp. Another was that so many of the claims made by Koprowski, by his former right-hand-man, Stanley Plotkin, and by others who had been involved with the vaccine or the vaccinations, were either misleading, or cleverly spun, or just plain wrong. The most worrying aspect was that a support team of largely Belgian and Congolese scientists reporting to Dr Plotkin had approached many of those interviewed in my book, and had persuaded several of them to withdraw, or modify, key elements of the statements they had previously made to me (and which I still have, recorded on tape). Most of these witnesses were given prepared statements to sign, and we were shown the original of one such statement, which was demonstrably false. The sender of the letter had even pencilled in the recipient’s name at the bottom, where he wanted him to sign. The recipient had refused to sign either this or a second statement that had been sent him, and he told me that the approaches represented a “dishonourable proposition”. In other instances, there was evidence that improper pressures had been placed on witnesses (that is, persons quoted by me in my writings) when they were subsequently approached by members of the Plotkin support group.

I had expected fair play at the Royal Society. I had been mentally prepared to stand up at the end and publicly hand over the investigation (and indeed offer my own source materials) to the scientific community, so that others could carry on the work. Instead, I encountered a cover-up. I decided to continue researching.

Meanwhile, Koprowski and Plotkin were not slow to claim victory, and the majority of scientists (innately inclined to believe their peers, rather than “a journalist” as I was immediately – and inaccurately – pigeon-holed) went along with them. In reality, relatively few had actually bothered to review the detailed evidence presented in The River, with its 850 pages of text, and 200 pages of endnotes and sources. It was easier simply to accept the word of colleagues who indignantly asserted their innocence. However, from those who took the trouble to read the book, I received only messages of support and encouragement, even if few working scientists were willing to come out publicly. (Several pointed out, rather ruefully, that this was a subject that could wreck a career.)

In April 2001, the brief reports by the labs that had tested the CHAT samples were published in Nature and Science, and both made a big splash of the findings in editorials and commentaries. Robin Weiss’s piece in Nature was titled “Polio vaccines exonerated”, as if I had questioned the safety of all such vaccines, and it ended with the claim that: “some beautiful facts have destroyed an ugly theory”. When, months later, I accosted Weiss about this, asking him for his evidence, he was unable to answer. He claimed instead that this was a phrase often used in lab meetings, an inversion of a more famous aphorism (by Thomas Henry Huxley). This latter assertion may be correct, but it did not make his sweeping claim any more acceptable – or true.

In his commentary, Weiss wrongly stated that the tested samples had “included the OPV batch (designated CHAT 13) used in Leopoldville [now Kinshasa, DRC]”. This confused the terms pool and batch which, for an experienced virologist, was an extraordinary detail to get wrong. To explain why requires a brief description of how oral polio vaccines were made in the 1950s. Passaging (or growing) a virus like poliovirus in different substrates, or tissue cultures (sheets of animal cells grown in vitro, in the laboratory), alters the pathogenicity of the virus, and OPV developers used this discovery to develop a weakened (or attenuated) version – one that would produce protective antibodies against polio in humans, but not the disease itself. The different numbered pools of CHAT vaccine such as pool 13 (each pool representing a poliovirus which had been subjected to a specific degree of attenuation) were all prepared at the Wistar Institute, or later at pharmaceutical houses in the USA and Belgium – and the tissue culture cells for this work generally came from the kidneys of macaques, a species of Asian monkey. What was crucial, however, was where and how the individual batches of those pools had been made. Some of these batches, I now realised, had been prepared in different labs and in different substrates. So Weiss’s description of CHAT 13 as a “batch” and not a “pool” allowed him to claim, wrongly, that the very same vaccine that had been fed in Africa had been independently tested – and “exonerated”.

As it happened, just a few days before these articles appeared, some colleagues and I had made a remarkable discovery in Kisangani (formerly Stanleyville), one which completely undermined the claims in Nature and Science.

Bill Hamilton and I had visited Kisangani in July 1999, he searching for stool and urine samples from local chimpanzees to test for SIV, and I trying to locate Congolese workers who had once been employed at Lindi camp, or the Stanleyville lab, the LMS. I found several who had worked at Lindi, including one witness with particularly good recall of events, but failed to find any who had worked at the lab. But now, just a year after Hamilton’s death, we had better luck.

We found three former lab technicians: one who had worked in the microbiology department of the LMS from 1956, and two others who had been employed in the virology department, starting in 1958. And just five minutes into his interview, one of the virology technicians revealed the detail that I had never before fully grasped.

Batches of CHAT vaccine had been prepared locally in Stanleyville.

This was the crucial detail that I had missed in The River. Until now, all the Belgian and American witnesses who had worked at the LMS, or who had been involved with the making or feeding of CHAT, had insisted that CHAT vaccine had not, indeed could not, have been made locally in Africa. They didn’t have the equipment, they said; they couldn’t possibly have produced a vaccine at a primitive lab like that in Stanleyville. And despite one or two intriguing “slips of the tongue”, which suggested that this was not the entire story, I had little choice but to believe them.

But now, suddenly, there was clear confirmation of what had really happened. The virology technician, Jacques Kanyama, explained that he had started working in the virology department of Dr Paul Osterrieth on February 12th, 1958, and he said that Osterrieth had already been making polio vaccine before his arrival. Each time a new order came in, he said, Dr Osterrieth would prepare fresh polio vaccine (in other words, a new batch). He described how Osterrieth would bring the vaccine from his sterile room, after which the assistants would divide it into phials. Sometimes the technicians also helped with the immunisations, and Kanyama recalled one particular episode when they took the vaccine across the river to Lukusa military camp, and vaccinated the soldiers and their families, giving each person a few drops by mouth. This was a crucial detail, because it not only established a chain of custody, but also identified the vaccine as CHAT, for Koprowski’s vaccines were the only ones given by mouth in the Congo at that time. It was important for another reason too, for the CHAT vaccination at Lukusa camp was recorded in a letter in the Belgian archives as having taken place on February 27th, 1958. (This was also Koprowski Day, the eighth anniversary of the day that the vaccine’s developer had taken the leap into the void, by being the first man in the world to give OPV to a non-immune subject – a seriously disabled six-year-old, who had to be fed through a stomach tube. Koprowski later referred to this child and 19 similarly handicapped vaccinees as “volunteers”.)

The key point now was: which primate tissue cultures had the Stanleyville doctors used to prepare the vaccine? Philippe Elebe had started work in April 1956 as a technician in the microbiology department (where Osterrieth had worked until the virology section opened in 1957). He told us that they had indeed been producing tissue cultures, and that he had been in charge of culture media – the balanced salt solutions, sera and antibiotics that are used to keep cultures alive and biologically “sterile” (free from known pathogens). We asked which species of primate had been used to make the tissue cultures, and Elebe’s reply was prompt. “Surtout les chimpanzés“, he said. “Mainly chimpanzees”.

After returning from Africa, I did further research. There had been no rules in the 1950s about which primate cells to use for growing polio vaccines: any species could be used, provided it made good cultures. Chimp kidneys apparently made “very good” cultures. But what I now discovered was that it had been routine practice for oral polio vaccine to be amplified locally, in different labs around the world. Some virologists, such as Albert Sabin, whose sugar lump OPV was eventually adopted for global use, acknowledged this fact in their publications. Others, such as Koprowski, did not. (It seems that he may not have wished to advertise how easy it was to obtain a sample of a live vaccine such as CHAT, perhaps from a vaccinee’s stool, passage it once more, and claim it as one’s own.) However, careful perusal of the papers written about the Polish vaccinations of 1959-60 by Koprowski’s collaborators, under Professor F. Przesmycki, reveals the truth, for the titre (concentration) of the CHAT vaccine had risen tenfold between the time of its arrival at the virology department of the State Institute of Hygiene in Warsaw, and the moment, a few weeks later, when the vaccine was diluted, and distributed to smaller labs around the country. Because vaccine titre decreases with time and temperature change, the only plausible explanation is that the titre had been boosted by further passage in primate cells in Warsaw, prior to dilution. The Polish scientists used macaques in their lab, so it is highly probable that they made their batches in macaque cells – and macaques are not naturally infected with SIV. This suggests why, of those seven million children fed Koprowski’s vaccines in Poland, none became HIV-infected as a result. The same factor applies to the million-odd persons fed CHAT elsewhere in Europe, and the 1,200 or so fed in the USA.

I learned that for trials in continents such as Africa (then at least two days from the US by plane), the standard practice was to fly a small bottle of the vaccine, packed in an ice-box, to the destination lab, where it was amplified in whichever primate cells were locally available. This meant that less vaccine had to be transported, and that vaccine quantity and titre could be boosted upon arrival. The higher the titre of the new batch, the more it could be diluted, and the more people could be vaccinated. By the second half of the 1950s, virologists based in South Africa were using African green monkey cells to amplify the Sabin vaccines, while their colleagues from French West Africa and French Equatorial Africa were using cells of the baboon (and perhaps other species too) to amplify the Pasteur Institute vaccines of Pierre Lépine. In Stanleyville, of course, they had the Lindi chimpanzees.

Over the last two years I have conducted further interviews with some of the Europeans who once worked at the LMS – not easy, because most such individuals are now firmly in denial. (Paul Osterrieth, for instance, recently posted a statement on the Web in which he contradicted several of his own previous statements, and made errors about known historical events. What was notable was his continued avoidance of the key issues: what happened to the chimpanzees, and to the polio vaccines.) Others, however, have been more open. By gentle and persistent questioning, I managed to get confirmations of each of the crucial parts of the story – and to get them on tape. This is not the time to reveal all the details, because doubtless further efforts will be made to encourage witnesses to retract, or restructure, their statements. But suffice it to say that the case is now clear: Koprowski’s polio vaccines were made locally in Stanleyville for a number of years, and the cells used for the great majority of the tissue cultures were those of the chimpanzee.

Ironically, a referee’s report on a powerful letter about the OPV theory which Bill Hamilton submitted to Science in 1994 reveals that the referee is well aware that the main risk of the theory being correct relates to “the possibility of local contamination by chimpanzee tissue in Central Africa”. Other details in that report reveal that the author is none other than Robin Weiss. Unfortunately, Weiss’s prescience was matched by his sensitivity to the political implications, for he seems to have voted against publishing Hamilton’s letter. His report reveals that he was also against testing old CHAT samples, because this “[would] not provide an answer”, and because the “lesson to help prevent further modern, possibly iatrogenic epidemics … is already made explicit.”

The new information about how CHAT was prepared for the central African trials does not prove that the vaccine started AIDS. But it lends a real urgency to the debate.

Over the last three years, various alleged “disproofs” of the CHAT hypothesis have been put forward by scientists, and supported by respected commentators like Dr Weiss. Yet not one of these disproofs stands up to scrutiny.

One such claim involved an attempt to calculate whether a potential contaminating virus such as chimp SIV could have survived the vaccine-making process, and concluded that the chances were trillions-to-one against. This is wrong. The tissue cultures used in Stanleyville, until at least mid-1958, were primitive Maitland-type cultures, which would have provided ideal substrates not just for attenuated polioviruses, but also for SIVs. (More sophisticated cultures involved the use of trypsin, an enzyme which also happens to inactivate most virions of HIV and SIV – but trypsin was apparently not used in Stanleyville until late 1958 or 1959.) At least some of these cultures also employed chimpanzee sera to nourish the cells, which means that there was substantial potential for recombination (the exchange of slabs of genetic material) between different SIV strains in vitro.

It has also been claimed, for instance by a prominent group of researchers led by Beatrice Hahn and Paul Sharp, that AIDS could not have started in the 1950s, because the first HIV infection (the so-called “Eve virus”) must have occurred back in the 1940s or 1930s. The inadequacy of such theoretical calculations has recently been revealed, for the model used was quite simply inappropriate for the purpose. In Science last July, the magazine’s leading AIDS correspondent, Jon Cohen, wrote about a “beautiful study” of rampant recombination in the spleen of an HIV-infected patient, which revealed that three-quarters of the individual HIV-infected cells contained more than one HIV variant – a “staggering” result. Cohen added that the study “raises serious questions about phylogeny trees that attempt to date the origin of HIV, all of which intentionally discard recombinants to make the data interpretable.” Another geneticist, Mikkel Schierup, has pointed out that all it would have required to generate the diversity of HIV-1 variants seen in the world today would be two different chimp SIVs which somehow recombined in humans. Such an event could have happened in vivo (following sex between human vaccinees, for example), or in vitro (for instance in polio vaccines cultured in chimp cells that were later fed to humans).

The Hahn group has also insisted that the closest ancestor of HIV-1, the pandemic strain, is the SIV found in chimpanzees from west central Africa, and that the chimp SIVs from the DRC and central Africa are only more distantly related. I believe that this is a dangerous claim to make, and not just because recent mitochondrial DNA analysis suggests that the chimps from these two regions should be redesignated as a single subspecies. Even now, there are only four available SIV sequences from the west central African chimps – and two from the central African chimps. The latter are indeed both slightly less closely related to HIV-1, but crucially they differ massively from each other, which emphasises the urgent need for extensive SIV testing right across the chimpanzee range. The 500-odd common chimps that were housed at Lindi (with some 80 bonobos) were collected from a vast area, embracing more than a hundred thousand square miles of the Congolese rain forest – and by good fortune, we happen to know that at least one chimp (which survived at Lindi for more than two years) originated from the west central African area. Because cages and play-cages were shared, just one such SIV-infected chimp could have caused widespread SIV infection throughout the colony. So even if Hahn’s hunch is right, it would not disprove the OPV theory. Furthermore, as Schierup has observed, the recombination of any two differing chimp SIVs (for instance in tissue culture) would be enough to give birth to the AIDS pandemic.

Perhaps the major battle-ground in this debate, however, relates to the early epidemiology of AIDS. I believe that this is the strongest argument in favour of the CHAT hypothesis. We know that CHAT vaccine was fed in at least 27 different places, all in the DRC, Rwanda and Burundi. I have found that 68% of all the earliest AIDS cases in Africa (and therefore, with minor exceptions, the world), and 76% of all the earliest HIV infections in that continent, come from the very same towns and villages where CHAT was fed between 1957 and 1960. However, at the Royal Society conference, Professor Weiss allowed only one epidemiologist to appear as a full speaker, this being Kevin de Cock, a Belgian-American employed by the CDC. De Cock separated my Congo data from my Rwanda-Burundi data, and claimed that the apparent correlations meant nothing. Recently, however, another statistician has devised a new software programme to analyse five competing scenarios for the emergence of AIDS in Africa. Full details are not yet in, but it seems that there is a good fit for only one scenario – OPV/AIDS. The correlations are apparently “highly significant”.

The most interesting counter-argument against OPV has been put forward by two American scientists, Preston Marx and Ernest Drucker. They take the cut hunter/natural transfer scenario (which theoretically could have occurred at any time in the last few million years, since the time that chimps and humans evolved from a common ancestor), and invest it with a necessary time-frame. They do this by proposing that there was an amplification factor, this being the arrival in Africa of disposable needles (which were none the less reused). Apparently needle deliveries to Africa experienced an exponential rise in the 1950s.

Marx and Drucker propose that the SIV-infected hunter or bushmeat-seller (or someone infected therefrom) went to a clinic and was injected with a needle that was then reused on somebody else. This process would then have been repeated a few more times, which potentially might have allowed the human-adapted SIV to become more pathogenic or transmissible. Theirs is a theory not of iatrogenic (physician-caused) origin, but of iatrogenic spread. It is the only version of “cut hunter” that seems even reasonably plausible, for otherwise cut hunter supporters have to rely on urbanisation as the factor that allowed a non-human primate virus that had recently passed to humans suddenly to explode, and begin its awful global march. In fact, they would require this to happen not just once, but four times, and almost simultaneously, because of the four different HIVs that have emerged and become established in Africa within the last several decades. (Phylogeneticists identify four separate outbreaks of HIV infection, relating to at least four transfers of primate SIV to humans. First there is the pandemic strain, HIV-1 Group M, with the “M” standing for “Main” group. Then come the minor outbreaks, which have infected between a few hundred thousand and a few dozen persons, and which are caused by HIV-2, HIV-1 Group O (for “Outlier Group”), and HIV-1 Group N (for “New Group”). HIV-2 is similar to the SIV of the sooty mangabey, a West African monkey, whereas all the HIV-1s are closely related to chimpanzee SIV.)

In fact, the minor HIV outbreaks fit rather well with the OPV theory, for it is known that experimental French-made polio vaccines were tested in the fifties in both French Equatorial Africa and French West Africa, which represent the epicentres of the three minor outbreaks. Among the primates the French were using for their research were chimps and sooty mangabeys.

The Marx/Drucker theory has been embraced with rather unseemly passion by many in the scientific establishment, even though it involves the medical profession playing a key role. This may be because the theory is non-specific, so no individual physicians or institutions can be held responsible. And there is also an unspoken subtext – that the physicians in question were probably not western ones. However, the reuse of unsterilised needles did not happen only in the Belgian Congo, so this theory is unable to explain the strong correlation between early HIV/AIDS, and the 27 known CHAT vaccination sites.

In short, the Marx theory is based on a temporal, but not a geographical, coincidence. One might, with just as much merit, propose that rock-and-roll, which emerged in the fifties, prompted more sex, more HIV spread, and thus an Elvisogenic epidemic.

In recent days, there has been a new spin on the needles debate, sparked by Professor David Gisselquist, who has been variously described as an anthropologist, an independent consultant, and an HIV specialist. He heads a group of American academics who conducted a survey of various epidemiological studies of HIV, which they combined with the rather contentious proposal that levels of sexual activity in Africa can be roughly equated with those in America and Europe. And they came up with a remarkable claim, which elicited much press coverage. In marked contrast to previous analyses, they concluded that 60% of all HIV spread in Africa was caused by unsterilised needles and unscreened transfusions, and only about 30% by sex. (The accepted ball-park figures were 10% for parenteral – or blood-borne – transmission and 80% for sexual, so this represented a sea-change.) Gisselquist has been quoted by Reuter’s as saying: “For the last 15 years, the AIDS establishment somehow got on to the notion that we need to scare people about sex to prevent HIV transmission”.

In reality, however, it seems to be Gisselquist who is scaring people, including some of his co-authors. I phoned one of them, whom I happened to have interviewed several years before, and was told that there had been disageements about the final published versions of the articles, and that some of the authors had had to withdraw their names from certain papers. There was also, I was told, concern about Gisselquist’s press statements. My informant told me that Gisselquist had “only moved across to the medical field two years ago”. Later, I checked on the Web, and discovered that before that he had been a “consultant at the World Bank”, an economist who wrote papers about how to save the Russian economy.

The Gisselquist group provides a long list of surveys they have examined, and impressive pages of mathematical formulae, but their research smacks of ivory tower theorising, and a lack of experience of the African epidemic on the ground. They highlight early HIV surveys conducted during 1984-8, but the conclusions of most persons who worked on AIDS in Africa during that period are very different. In Uganda, which was probably the first country in the world to experience a visible community-wide AIDS epidemic, almost every survey from 1985 onwards revealed an age-prevalence pattern comprising intermediate levels of HIV-1 infection for 0-to-4-year-olds (presumably largely caused by perinatal spread), which plummeted to virtually zero for 5-to-14-year-olds, and then rose steeply for the ages of 15 to 45 for women, and 20 to 55 for men, before tailing off to zero for older individuals. Yet all age groups and both sexes would have experienced comparable levels of unsterile injections and unsafe transfusions. This “Christmas tree” pattern, which was recognised right across the continent in the 1980s, is strongly suggestive of a pathogen that is spread largely by the sexual route, with only minor roles played by perinatal and parenteral spread. Another powerful clue is the fact that HIV infection levels among Ugandan teenage girls were often many times higher than among teenage boys, which parallels the earlier onset of sexual intercourse for African females.

The Gisselquist co-author with whom I spoke told me his personal belief was that 20% to 30% (not 60%) of African HIV might be transmitted through unsafe medical practices. My own belief (based on many years of studying African epidemiological surveys) is that parenteral spread may have increased in importance since the start of the epidemic, and that nowadays it might cause between 10% and 20% of new infections. I would certainly defend the principle of debating such issues, for public health decisions must be based on sound information and data. And by all means let us fight to improve the quality of medical care and condom provision in Africa and elsewhere, and thereby hopefully reduce the transmission of HIV and other pathogens (whether by dirty needles, or unprotected sex). But most of those who have studied the African epidemic at close range believe that it is Gisselquist’s estimates that are speculative, and that some of his public utterances are simply irresponsible, given how many people are eager to hear, dying to hear, that unprotected sex is not that dangerous.

Of course, the more publicity that is given to claims that dirty needles are responsible for most of the HIV spread in Africa, the easier it becomes to promote the idea that dirty needles might also have sparked the epidemic. And there is clearly some linkage between the two theories, for one of Gisselquist’s co-authors is Ernest Drucker.

What is undeniable is that over the last two or three years a substantial body of scientists and medics, many from the USA, seem to be keen to promote an explanation for the origin of AIDS that, though avowedly iatrogenic, caused by the actions of physicians, involves no specific individuals or governments. No names, no scandal. Nobody held to account. No law-suits.

The arguments, the denials and protestations will sputter on for some time, but I firmly believe that over the next few years it will gradually come to be realised that the pandemic of AIDS was sparked by the large-scale field trials of an experimental polio vaccine – trials that employed African “volunteers” as guinea-pigs. I think that more and more people will begin to question whether this might be the most memorable and awful own goal yet scored by Homo sapiens, (or H. sapiens iatros).

Whether this scenario will ever be proved is debatable. Certainly a vigorous campaign of opposition and defence has been mounted, one that has the air of being coordinated. But the prospects for proof may be somewhat less unlikely than they at first seemed. There is much more supporting evidence than can be printed here. And in the meantime, various further tests are underway.

But if the OPV theory should come to be proven, then where should responsibility lie? Surely not just with Paul Osterrieth and his former LMS colleagues – for it is inconceivable that Osterrieth (who trained in tissue culture techniques at the Wistar in late 1957) would have grown the vaccine in chimp cells without the express approval of the then-director of the Wistar, Hilary Koprowski. But in that case the buck would go further still, for Belgium, as the colonial power, approved the CHAT field-trials. Moreover, various archival documents reveal that these trials, and the programmes of research at Stanleyille and Lindi, were being quietly supported and funded by various American institutions, most notably the Public Health Service.

An immense, horrific tragedy is unfolding in Africa and around the world. Sometimes we give it a few minutes as it passes uncomfortably across our TV screens. And sometimes, preoccupied or faint-hearted, we look the other way.

Tens of billions of dollars are now being devoted to regime change in the Gulf. Is it not time to ask when some of those billions will instead be allocated to the global fight against AIDS – the origins of which can be traced back to well-intentioned people in the same country that now spearheads the fight of “good” against “evil”?

Upon inspection the world’s new emperor, just like the fictional one, is looking rather underdressed.

The Lincei proceedings have just been published as “Origin of HIV and Emerging Persistent Viruses” [ISBN: 88-218-0885-8]. They include Ed Hooper’s extended essay, “Dephlogistication, Imperial Display, Apes, Angels and the Return of Mr Emile Zola”, which is also available on line, at

Background notes

Oral infection

It has sometimes been claimed that people do not become HIV-infected by the oral route. This is demonstrably wrong, as evidenced by the gay men who became infected after having only oral sex, and by the several recorded instances in which babies seroconverted during infancy – not through contact with HIV-negative mothers, but through being breast-fed by HIV-positive wet nurses. All mucosal cells, including those of the mouth and throat, represent potential portals of entry for the HIVs and SIVs, and the situation is exacerbated if there are oral lesions, such as those caused by teething or mouth ulcers, which lesions are packed with HIV/SIV target cells such as lymphocytes and macrophages. (Macrophages, which – unlike lymphocytes – survive and replicate in culture, look ever more likely to be the key cells in the process of infection through a SIV-contaminated OPV.)

Problems for the natural transfer theory

There is a disparity of place between the range of the cut hunter supporters’ mooted chimpanzee host (Pan troglodytes troglodytes, which is almost exclusively found in Cameroon, Gabon and Congo Brazzaville, all formerly part of the French colonial empire) and the AIDS epicentre (which is situated, as all parties now apparently concede, in the DRC, the former Belgian Congo). The “cut hunters” seek to explain this disparity by proposing that the hunter or bushmeat-seller who, they say, represented the point-source of the epidemic (or an infectee of same) may have migrated from somewhere in the troglodytes zone on the north bank of the Congo river to Leopoldville in the Belgian Congo (now Kinshasa, DRC) on the south bank, where, they postulate, the now human-adapted virus, which they term the “Eve virus”, began to adapt and spread. Their theory of origin therefore seems to require at least three quite separate steps: (a) for the key infectee to have migrated (in around 1930 or 1940, according to their time-frame), at least a hundred kilometres southwards, from a French colony to a Belgian, to spark the epidemic in Leopoldville; (in fact, the latest estimates of the site of the viral crossover by the Hahn school place it in southern Cameroon or northern Gabon, which would require a migration by the index infectee of at least 400 kilometres); (b) for the index virus that arrived in Leopoldville to somehow (by a process that is not yet explained) to diversify into at least ten distinct subtypes over the next 20 to 30 years; (c) for the onward spread of these various HIV-1 subtypes not to begin until the 1960s or early 1970s; and to occur not northwards or southwards from Leopoldville/Kinshasa, but only eastwards, to those towns and villages in the Congo, Rwanda and Burundi for which there is retrospective evidence of HIV-1 infection in the late 1970s. The cut hunter supporters have, therefore, to invoke quite a lot of coincidence to explain the location of the earliest recorded AIDS cases and HIV-1 infections. If one employs the basic scientific principle of parsimony, then the OPV theory (which postulates that different subtype variants of SIVcpz/HIV-1, which had evolved through in vitro recombination, were introduced to humans in Leopoldville and other sites in the Belgian Congo and Ruanda-Urundi between 1957 and 1960) looks considerably more plausible.

More detail on pools and batches

Passing a virus such as poliovirus through different animals, or passaging (growing) it in different substrates or tissue cultures (sheets of animal cells grown in vitro, in the laboratory) alters the pathogenicity of the virus, and what polio vaccine-makers are looking for is a weakened, or attenuated version that will produce protective polio antibodies in humans, but not the disease itself. (Unlike injected polio vaccines, which almost exclusively use killed polioviruses, oral polio vaccines employ living, attenuated polioviruses.) A “pool” of OPV describes material produced at a specific level of attenuation – for instance, “Pool 9” might indicate a poliovirus that has been weakened by being passed 28 times through chick embryo tissue culture, and eight times through monkey kidney tissue culture. (In most American and European virology labs in the fifties, “monkey kidney tissue culture” generally meant kidney cells from macaques, a species of monkey found in India and the Philippines.) By contrast, a specific batch of Pool 9 would describe a quantity of vaccine that had been prepared from that pool on a specific date in a specific lab: in other words, in a single production run. In practice, batches are prepared by taking a small quantity of the vaccine pool (or a batch made from that pool), and amplifying it by a final passage in some variety of locally-available monkey kidney tissue culture.

The name of the vaccine

CHAT is an unusual name for a polio vaccine, and Koprowski and Plotkin have long maintained that it represents either the initials, or an abbreviation, of the name of the young patient from whose stool the attenuated CHAT virus was first isolated. I managed to locate the father of that patient, whose surname was Charlton. This offered support to Koprowski’s account, even if it did raise the question of why he chose CHAT, rather than CHA or CHAR. However, the suspicion persists that there may also have been a sub rosa meaning. One of the OPVs developed by Albert Sabin in 1956 incorporated “Ch” in its name to indicate that the vaccine virus had been passed through a chimpanzee, so one wonders whether (at least for those in the know), CHAT may not also have meant “CHimpanzee Adapted and Tested” or “CHimp-ATtenuated”, which the latest evidence reveals would have been accurate descriptions of at least those versions of CHAT vaccine that were fed to unsuspecting “volunteers” in Africa.