Review of The Origins of AIDS by Jacques Pepin [C.U.P. 2011]
“The Origins of AIDS” by Jacques Pepin [Cambridge University Press], which came out in October 2011, has received a fair amount of attention in the press, almost all of which has been complimentary. I have a rather different take on the book.
I believe that the book is pleasantly and fluently written and is mostly well-researched. It contains a wealth of valuable information about how unsterilised needles and syringes may have helped spread HIV in Africa in the latter half of the twentieth century, in the early days after the origin of the pandemic, in other words after the ancestral simian immunodeficiency virus (SIV) crossed from chimpanzees to humans.
This makes it all the more surprising that the two chapters (out of fifteen) that deal directly with the alleged subject of the book, the origins of AIDS, are so poorly researched and executed.
Having acknowledged on page 2 that the only previous book to have dealt with the subject was my book, The River (Little Brown; 2000), Pepin later spends 3 pages (50 to 53) attempting to explain why the oral polio vaccine (OPV) hypothesis (which my research as reported in The River found to be the most viable) can be dismissed because, as he alleges, “there is now overwhelming evidence that it did not happen”.
The evidence he claims to rely on consists of a series of alleged “disproofs” of the OPV theory that have been repeatedly promoted in the pages of certain scientific journals, notably Nature and Science, since the Royal Society conference on “Origins of HIV and the AIDS Epidemic” in September 2000. Almost all of these alleged disproofs have come from one or both of the following groups: (a) a group of medical researchers (including Hilary Koprowski, Stanley Plotkin and Paul Osterrieth) who were involved in developing, preparing and staging human trials of CHAT oral polio vaccine (OPV) in the 1950s, and (b) a group of microbiologists and molecular biologists featuring Beatrice Hahn, Paul Sharp, Bette Korber and Michael Worobey, who promote the hypothesis that HIV was acquired by humans some decades earlier than the 1950s, in the course of the hunting and butchery of chimpanzee bushmeat.
Most of Pepin’s alleged disproofs are addressed elsewhere in this posting, in the “Quick Guide”. However, let me address three other “dispoofs” that he puts forward.
a) He claims that the Laboratoire Medical de Stanleyville (LMS) was simply not modern or advanced enough to produce any polio vaccine in the late 1950s. This claim is based on the statement made by Paul Osterrieth at the Royal Society conference that the LMS was too primitive to make vaccine, and that he did not succeed in making any tissue culture until mid-1958, roughly five months after the start of the Ruzizi Valley trial – and that then it was made from baboons. But we have an eye-witness account from one of Osterrieth’s African assistants stating that Osterrieth was “making polio vaccine” in his Virology Laboratory by mid-February, 1958, before the start of the Ruzizi trial, and this account is supported by a second technician who was working in the lab of the director, Ghislain Courtois, next door. Moreover, what is at issue here is not producing a polio vaccine from scratch; it is merely preparing a batch of vaccine locally, which involved nothing more than placing a sample of the vaccine that had arrived from the US into a locally-prepared tissue culture, made from chopped chimp kidneys, nourished with chimp serum and artificial media, and kept bacteriologically sterile by the addition of penicillin and streptomycin. This local preparation of vaccine both kept the original vaccine alive, and improved the titre (concentration) and quantity of the product. It appears to have been standard practice all around the world in the mid to late 1950s. Local batches of polio vaccine were made in places as far afield as South Africa, Poland, the USSR, China and Vietnam. Most of these places made their batches in a tissue culture prepared from rhesus or cynomolgus macaques from southern Asia, but in South Africa, for instance, they used African green monkey cells from the beginning – because they were locally available. Another relevant detail is that there is documentary evidence that the new LMS virology lab, which only formally opened in October 1957, had in fact opened for business at the end of 1956, and was in reality a modern, well-equipped, air-conditioned lab, with a separate room for undertaking sterile procedures. I said at the time of the RS meeting that the statements by Professor Osterrieth sounded far-fetched and even absurd; I now have documentary evidence that they were false.
b) Pepin claims that I confused conditionnement, which refers to repackaging, in this case to distributing vaccine into smaller bottles, with the process of local vaccine preparation. This is untrue. I asked Osterrieth about what conditionnement meant in 1994, and after that I was quite clear about it. Moreover I reported this clearly on page 564 of The River. The evidence for local vaccine preparation (which is extensive) is quite separate.
c) Pepin claims that after The River was published, I “changed [my] hypothesis somewhat and suggested that the Stanleyville laboratory had produced batches of the vaccine locally”. This is strictly speaking correct, but is misleading, because it avoids stating what I have made clear: that in The River I had little choice but to accept as true the final accounts about where the vaccine was made as given me by doctors Koprowski, Plotkin, Ninane and Osterrieth. (I did add a hypothetical account on pages 790-791 of what would be the implications if the vaccine had been made locally in Stanleyville, but that was as far as I could reasonably go at that point.) What followed was anything but the “flip-flop” that Pepin implies. In the months following the Royal Society conference, the first hard evidence came to light suggesting, and then proving that the accounts given by doctors Koprowski, Plotkin, Ninane and Osterrieth were untrue, and that batches of CHAT vaccine had been prepared locally in Stanleyville. (I immediately reported this evidence in my paper “Dephlogistication” at the Lincei conference in Rome in September 2001, but in his summation at the end of that conference, Robin Weiss simply ignored the fresh evidence that I had reported. The rest of this episode has been reported elsewhere, but the actions of Weiss in both London and Rome demonstrate that he has shown a conspicuous lack of even-handedness throughout his involvement in the origins-of-AIDS debate.)
In summary, Pepin’s claim that the OPV theory “can be firmly rejected” is based on false evidence and reasoning, and is demonstrably incorrect.
Because Science and Nature have repeatedly rejected every riposte that I and others have made to articles written by members of the bushmeat school since 2000, I have been restricted to publishing such ripostes on the www.aidsorigins.com web-site. Readers of this site (which there is evidence to show include many of the bushmeat proponents) are aware of my arguments that not one of the alleged disproofs of OPV/AIDS has scientific merit.
But Dr Pepin simply ignores what I have written, both at the Royal Society and thereafter, and instead briefly summarises half a dozen arguments which allegedly explain why the OPV hypothesis “can be firmly rejected”. In other words, at the very core of his own book Pepin is merely parroting the alleged disproofs of OPV/AIDS offered by one very partisan side of the origins debate, without offering any examination of the arguments. He’s already made up his mind, and he doesn’t waste any pages explaining the reasons for his convictions.
Let me give an example of the inadequacy of Pepin’s analysis. In Chapter 3, he gives an account of the phylogenetic dating of HIV using the model of a molecular clock (a clock that is calibrated to the mutation rate of HIV, meaning that you can supposedly place dates on the major events in the evolution of that virus). On pages 39 and 40, he correctly points out the central shortcoming of that method. He says that the principle of molecular clocks “is based on an assumption that the rate of genetic change is fairly constant over time”, and that when making calculations based on molecular clocks “all inter-subtype recombinant viruses must be excluded. This works well as long as the recombinants are identified, which is not always easy.” However, that is the last comment he makes on the subject.
In short, Pepin correctly identifies the inherent flaw in all phylogenetic dating analysis of HIV. What he fails to point out is that in an AIDS patient who is dually infected (with two different strains of HIV), at least 90% of the evolution of the infecting HIV-1 strains comes about as a result of recombination rather than mutation. HIV, a lentiretrovirus, is innately recombinogenic, and this highly unusual quality means that using the molecular dating approach for this virus is inherently flawed. (By contrast phylogenetic dating works fine for DNA viruses such as smallpox, which evolve almost wholly through mutation.) However, Pepin simply accepts the assurances of the molecular biologists that they have succeeded in their task of excluding recombinant viruses from their databases. The truth is very different – for it is impossible to identify recombinant strains of HIV and SIV when the recombination has occurred early in the history of the virus. Pepin fails to recognise this, or to notice that the bushmeat proponents are in trouble about this. In fact, they have now begun writing in terms of “relaxed molecular clocks” (an interesting construct!), and wrestling with an unresolved disparity of several orders of magnitude between the presumed evolutionary rates of the SIVs and their primate hosts. This in itself gives a clear indication that their dating of key events (like the chimp-to-human transfer) is, at the very least, open to question.
Michael Worobey even acknowledged this in a paper published on-line in 2009; [“Dating the Age of the SIV Lineages That Gave Rise to HIV-1 and HIV-2”, J.O. Wertheim and M. Worobey; PLoS Computational Biology; 2009; 5 (5); e1000377]. The abstract ended with the sentence: “Our results suggest either that SIV is a surprisingly young viral lineage or that SIV and, perhaps, HIV dating estimates are seriously compromised by unaccounted-for biases.” However, he is not suggesting that the chimp-to-human transfer dates might have come down into the 1950s. Instead, he seems to be debating whether all primate SIVs might be quite recent (merely thousands to ten thousands of years old), or else, conversely, that the HIVs might be much older than previously thought. Everything, it seems, is up for grabs. The Discussion reveals that his timing estimates were generated by combining the molecular clock results with “a more biologically plausible model of rate variation among lineages”, and he states that analyses were performed using something called an “uncorrelated lognormal relaxed molecular clock”. What is remarkable is that scientists like Worobey don’t seem to realise that by combining statistical data with that their own preconceptions of what comprise “more biologically plausible models of rate variation”, they merely enshrine their own biases into the results.
The HIV geneticists like to think in terms of Most Recent Common Ancestor (MRCA), which for pandemic AIDS is thought of as the year in which the common ancestor of all the HIV-1(M) variants seen in the world today existed. In Molecular Clock Land, you can then back-calculate even further, by postulating a date for the cross-species transfer, which is generally assumed to have preceded the MRCA date by at least ten years: a typical gestation period for AIDS. (Often their estimation of the gap between transfer date and MRCA is much longer than 10 years. But that’s the point when you start getting into the game of estimating dates: you can come up with any old rubbish, and stand a decent chance of grabbing a headline or two.) One of the more delightful conclusions in the aforesaid Worobey paper is that the Most Recent Common Ancestor of chimp SIV first existed in 1492, that the virus stayed in chimps for 403 years, and that the MRCA of HIV-1(M) came into existence in 1895. (It will be noted that this is 13 years earlier again than his previous guess of 1908.) One also notes that according to this version of events, the arrival of SIV in chimps occurred in the same year that Columbus was sailing the ocean blue, and wonders whether this was a Relaxed Molecular Coincidence or a deliberate seeking after headlines. In any case, I believe that the shorthand for this sort of thing is GIGO: “Garbage In: Garbage Out”.
But back to Pepin. Basing his work on phylogenetic dating analysis, Pepin chooses 1921 (with a probability range of 1908 to 1933) as his MRCA date for HIV-1(M). In shorthand, 1921 can be thought of as his date for when the new virus began to spread in humans.
To be fair, Pepin does note that the addition of one single isolate to the database – Worobey’s sample from 1960 – altered the estimated MRCA date by ten years, from 1931 (the previous estimate) to 1921, and comments: “This gives us an appreciation of the lack of certainty” of such calculations. In fact, the estimated change in the crossover date due to the inclusion of Worobey’s 1960 sample was even more than that: 23 years. This is because Worobey’s eventual calculations, as reported by the authors of Tinderbox, were that the MRCA of HIV-1(M) was 1908, with a range from 1884 to 1924.
Pepin is quite correct to highlight the flimsiness of that MRCA date. However, he never follows through on the shortcomings of phylogenetic analysis of HIV-1. This is probably because, like most people, there comes a point where he begins to find the more arcane aspects of the argument quite hard to follow. At this point, most people just accept the word of the geneticists that their account of what they are doing can be trusted, and that that they have got everything covered. This is unfortunate, because in reality there are several indications that the geneticists’ dates for the beginnings of HIV-1(M) are in disarray. What appears to be crucial from their perspective, although they will never admit it, is that their MRCA estimate falls some years earlier than the OPV trials in the 1950s.
By contrast, in Chapter 4 of his book Pepin does make an important contribution to the origins debate by attempting to quantify the risk of humans acquiring chimpanzee SIV through the hunting and butchery of chimpanzee bushmeat. Pepin says “to keep things simple” he will use 1921 as the date of the first HIV-1(M) virus. On the basis of past surveys conducted in Cameroon and elsewhere in Africa, he then estimates that 1,350 adults living in the Pan troglodytes troglodytes area of central Africa in 1921 might have been exposed to chimpanzee blood at least once in their lives, of whom 80 adults might have been exposed to SIV-infected chimp blood at least once in their lives. On the grounds that 0.3% of health care workers who suffered needle-stick injury with HIV-1-infected blood in the 1980s (before antiretroviral drugs were widely used in that group) got infected with HIV-1, he makes “an educated guess” that between three and ten times as many persons (between 1% and 3%) exposed to infected chimp blood due to hunting or cooking might thereby have become infected with SIV.
He thus concludes that in 1921 the total number of persons in the world infected with SIVcpz-infected blood would have been between 0.8 and 2.4. Remember, this is a grand total based on lifetime risk, not an annual total of new infections.
However, if we take Pepin’s calculations a little further, it quickly becomes apparent that this figure presents problems for the members of the bushmeat school. Remember that for many years they have been asserting that the crucial transfer of SIVcpz to humans occurred in south-eastern Cameroon, where they claim that a hunter or butcher became infected with SIVcpz and then he or she (or someone infected by them) travelled down to Leopoldville, 600 miles away in the Belgian Congo (now Kinshasa in the Democratic Republic of Congo, DRC), and sparked the global AIDS pandemic. The area of south-eastern Cameroon that they specify (let us call it the “mooted transfer zone”) is a small part in the south of East Region, which Wikipedia describes as “the most sparsely populated of Cameroon’s ten [regions]”, providing just over half a million (1 in 38) of Cameroon’s current population of 19 million people. The southern areas of East Region that the bushmeat theorists specify as the “transfer zone” represent only a small proportion of the region’s area, but to be on the safe side let us assume that they contain half the region’s population, or roughly 1 in 76 of Cameroon’s people. Since the total population of Cameroon in 1921 was around 3.31 million, this would suggest that about 43,600 people (mainly Babinga pygmies) were living in the “mooted transfer zone” in 1921. This represents just 1.89% (or about 1 in 54) of the total figure of 2.3 million people that Pepin proposes were living in the region of the Pan troglodytes troglodytes subspecies of chimpanzee in that year.
Pepin argues that between 0.8 and 2.4 people were infected with SIVcpz-infected blood in 1921. This can be reinterpreted as odds of between 22 to 1 and 67 to 1 against an HIV-infected person existing in the “mooted transfer zone” in south-eastern Cameroon in 1921.* Already these are impressively high negative odds.
Now we come to the second part of the bushmeat theory: that the virus somehow quickly transferred to the nearest large metropolis, this being the city of Leopoldville (nowadays Kinshasa). So how many of these 41,200 Cameroonians from the “mooted transfer zone” would be expected to go anywhere near Brazzaville or Leopoldville in their lifetimes? Pepin’s own figures state that 127,750 men were conscripted to work on the construction of the Mayumbe section of the CFCO railway from Brazzaville to Pointe Noire over a 14-year period (1921-1934), this being an average of just over 9,000 men per year. However, according to Pepin these recruits came from the countries now known as Congo Brazzaville, the Central African Republic and Chad, in what used to be Afrique Equatoriale Francaise (AEF), but not from Cameroon, which was always a separate country until the time of Independence in 1960.
My own educated guess is that in 1921 an absolute maximum of 10% of the local population of south-eastern Cameroon would be expected to travel as far as Brazzaville or Leopoldville (some 600 miles away) in their lifetimes. (African travel, especially across borders, was not a common thing in 1921, unless it was promoted by the state. The true figure may be nearer 1%, but let me give the bushmeat people the benefit of the doubt.) The odds against a chimp SIV-exposed person from south-eastern Cameroon travelling to Brazzaville or Leopoldville to infect others with HIV thus become far more significant: between 225 to 1 and 675 to 1 against. Once again, let me give them the benefit of the doubt, and assume that the former figure is reasonable. Suddenly the south-eastern Cameroonian scenario that the bushmeat people have been promoting for years is revealed for what it is: an extremely far-fetched hypothesis. These odds of 225:1 against lie well outside the 20 to 1 against odds that represent the normally accepted lowest confidence intervals (95% CI) for proposing a hypothesis.
Even the chance that an initial south-eastern Cameroonian infectee in around 1921 would infect someone else locally who then infected a third person (or via that person, a fourth person) who later travelled to Brazzaville or Leopoldville and infected others has inherent problems. Remember, there is no epidemiological evidence whatsoever to support the hypothesis of an early outbreak of AIDS (one that died out locally, but only after HIV had “escaped” to Leopoldville) having occurred before the 1980s in that south-eastern corner of Cameroon, or indeed anywhere in Congo Brazzaville, the country that lies in between southern Cameroon and Leopoldville. The three other outbreaks of HIV-1 infection (those caused by Group O, Group N, and the still-unconfirmed Group P) all appear to have occurred in rural areas of the old AEF and Cameroon, around their assumed transfer points (whether those transfers occurred through the handling of bushmeat or the administration of chimp-based vaccines). Why should Group M have behaved so dramatically differently?
It is worth pointing out that the Hahn group have long been reticent about the precise degree of similarity that exists between their south-eastern Cameroonian chimp SIV and pandemic HIV-1. However, analysis provided in January 2012 during an email exchange with a member of one of the 5 or 6 labs that produce regular papers about the phylogenetic analysis of HIV-1 suggests that there is roughly 85% similarity across the genome between the AIDS pandemic strain, HIV-1 Group M, and the closest SIV from a south-eastern Cameroonian chimpanzee. (In very broad terms, this compares to about 80% similarity when one compares the AIDS pandemic virus to other Pan troglodytes troglodytes SIV strains and about 70% when comparing to most Pan troglodytes schweinfurthii SIV strains.)
In fact, this 85% similarity is not nearly close enough to prove direct ancestry (which is probably why the Hahn group has kept so quiet about the precise details of the sequences). During the course of a lengthy email exchange, the HIV geneticist referred to above recently confirmed my suspicions. He explained that the closest SIV found in a Cameroonian chimp is actually still “quite distant from” pandemic HIV-1, so Cameroon might very well not be the “hearth of AIDS” after all. He added that the degree of similarity (85% is my estimate of the similarity along the whole sequence; he declined to give an estimate) probably means that the actual troupe of chimps that gave birth to HIV-1 has not yet been sampled, or that it has become extinct since the early part of the last century. (He is assuming that it was one member of a specific troupe of chimps that gave birth to HIV-1; as explained elsewhere, I do not believe this to be the case, unless one chooses to think of the 500 or so diverse chimpanzees and bonobos housed at Lindi as a “troupe”.)
Why does the Hahn group so consistently make claims that it cannot support? As my geneticist correspondent explained in a recent email: “The Hahn group in general holds their sequences very private until they can get a ‘big paper’ out in Nature, Science, or whatever. They’ll show posters, and publish hints in journals that don’t require them to make the sequences public, but not ‘show the goods’ until they’ve got the story all wrapped up.” On one level this is frank, but it also features a fairly sympathetic interpretation of their tactics and motives.
A good example of this is happening right now. In 2010 the Hahn group presented a poster at a retrovirology conference [Li Y., Sharp P., Worobey M., Hahn B. et al.; “Molecular Epidemiology of Simian Immunodeficiency Virus in Eastern Chimpanzees and Gorillas”; 17th Conference on Retroviruses and Opportunistic Infections; 2010; poster B-108] that confirmed what I have always argued: that SIV is found right across the range of Pan troglodytes schweinfurthii (Pts) in northern DRC (the former Belgian Congo). I had heard on the grapevine some seven years ago that the Hahns were getting SIV-positive findings from DRC chimps, and I have frequently asked (sometimes on this site) why nothing has yet been published. The poster reports that 1670 faecal samples from Pts chimps had been collected, that 295 of them were found to be SIV-positive, and that they obtained genetic sequences of SIV from 96 of them, representing at least 77 different SIV-infected animals. No estimate for the prevalence of SIV in Pts chimps is given, although from these figures it appears to be very similar to the 5.9% that the Hahn group estimates for Ptt chimps from Cameroon (Pepin, page 29). The poster states that the Pts SIV sequences “exhibited considerable genetic diversity, but all fell within the SIVcpzPts radiation”. In short, the authors are claiming that all the viral sequences found in Pts chimps are genetically distinct from Ptt SIV sequences. However, they have not revealed any details about the new Pts sequences. Two further years have passed and still nothing has appeared.
For eight years the Hahn group have relied on Worobey’s Parisi Forest sequence to argue (wrongly) that the OPV theory has been disproved, and even now, when they have extensive data on SIV in Pts chimps from the DRC, they still don’t publish. One has to ask whether this chronic tight-fistedness with information might be related to their having some problems with the data. Maybe there are certain details here which they would prefer not to be made public.
This way of doing science seems to reflect the phoney science of the 1908 (or is it 1921?; or 1931?; or 1895?) MRCA date. The technique the Hahn group repeatedly employs is to claim that they have disproved the OPV theory when they have not, and for Nature and Science to suppress all criticism of their techniques, thus buying them time. The “false disproof” approach (which is good enough to convince most people – including most scientists – that they know what they’re talking about) effectively allows the Hahns and the Worobeys to hold the fort until (hopefully for them) they can contrive some better argument in the future. This is science controlled not by the search for truth, but by what the grandees of science consider to be politically desirable.
Beatrice Hahn and her supporters (like Paul Sharp, Michael Worobey and Bette Korber) want to have things both ways. They make huge, sweeping claims at press conferences about 1908 MRCA dates and pandemic AIDS having been born in south-eastern Cameroon, but then quite frequently fail to release the sequence data that supports their claims. And when the data is released, it quite often turns out not to contain what they claim it contains, as in the case of the alleged Cameroonian hearth.
All these subtleties are missed by Dr Jacques Pepin, who either doesn’t understand, or doesn’t choose to understand. On page 221 of his book he claims that the SIV of Pan troglodytes troglodytes chimps is “genetically identical to HIV-1”. As it stands, this claim is simply untrue. The SIVcpz-Ptt isolate that is genetically closest to the human virus is not 100% similar to HIV-1(M), but 85% similar.
In reality, there is no hard evidence to support the claim that the crucial transfer of chimp SIV to humans took place in south-eastern Cameroon. The Cameroonian chimp SIV is merely the closest match to date to the human pandemic strain. Even if one assumes the bushmeat theory to be correct, then the key crossover might have taken place elsewhere in the Pan troglodytes troglodytes range. Or it might even have taken place in Pan troglodytes schweinfurthii range, or in the range of Pan paniscus (the pygmy chimp, or bonobo). Since not all chimp and bonobo troupes have been sampled, the one that carries an SIV that most closely resembles HIV-1(M) might well have become extinct since the transfer occurred. (And in any case, of course, the OPV theory proposes an entirely different chain of events.)
As an aside, no SIV has been reported from the pygmy chimp (Pan paniscus), although for many years only about 30 had ever been sampled. The Hahn group recently claimed that some 150 pygmy chimps have now been sampled, without any evidence of SIV being found. However, this does not prove that Pan paniscus (of which 86 were apparently housed at Lindi camp) is not infected with its own SIV. The question has to be asked: if one of the more fanatical bushmeat scientists did actually discover an SIV that closely resembled HIV-1(M) in a pygmy chimp, would he – or she – necessarily report it to the world? At present, since they have monopolised all the primate investigations in central Africa for at least the last 12 years, we may have a situation where the poachers are in charge of the hen-house.
But there is an even more basic point that needs to be made about the genetic sequencing of SIVs from African primates. If the OPV theory is correct, then it might well not be the chimp SIV that is genetically closest to HIV-1 that represents the source of the pandemic. The “closest match” argument may well be a red herring. I believe, of course, that the vital viral transfer of chimp SIV to humans involved events that took place at the Laboratoire Medical de Stanleyville (LMS) in the old Belgian Congo, and at more than 30 vaccination sites in the Belgian Congo and Ruanda-Urundi in 1957-1960. There are four main reasons for this: (a) since the 1990s there has been evidence suggesting that at least some Ptt chimps were present at Lindi, in addition to 300 to 400 Pan troglodytes schweinfurthii and an alleged 86 Pan paniscus; (b) about 4 years ago I revealed that there was documentary evidence that at least one Pan troglodytes troglodytes chimp was present at Lindi Camp, for a period of up to 32 months; (the key source for this is: Acta Cardiologica; 1965; [no volume number]; Supp. XI; 283-297); (c) it may well be that only in the chimpanzees and bonobos of Lindi Camp, and in the tissue cultures and vaccines prepared at the LMS, were there opportunities for in vivo and in vitro mixing of different chimp SIVs, to produce exactly the range of HIV-1(M) subtypes seen in the AIDS pandemic today, and (d) I am still working on further lines of enquiry. In other words, there is more information still to be revealed.
Because the alleged, but false disproofs of the OPV theory that have been published by such as Hahn, Sharp, Worobey and others are the only versions of the genesis of AIDS that are published by Science and Nature, I have decided instead (for the time being) to publish my own refutations to this disinformation in articles posted on this web-site: www.aidsorigins.com. However, it seems that these on-line articles might have been better received by the public than the bushmeat proponents would have you believe. The last time (before its coverage of Pepin’s book; see below) that the New York Times published a major article on the subject of the early history of AIDS, in November 2010, it involved Michael Worobey’s paper on SIVs on the island of Bioko, off West Africa. [See “The Bushmeat Gang: The Gang That Couldn’t Tell The Time” on this web-site.] In the 24 hours that followed publication of that article, 101 comments were logged on the New York Times web-site, few of which offered support to Worobey, although 20 of them made positive reference (either directly or indirectly) to the OPV theory. This is field evidence that although some members of the medical establishment might wish otherwise, this debate is far from over.
Finally, after that long digression, let me get back to Pepin’s book. Apart from its blanket rejection of the OPV theory, there is one other striking detail about the origin of AIDS that it alleges. It was highlighted by the journalist who praised Pepin’s book so highly in the New York Times [“Chimps to Humans to History Books: The Path of AIDS”, by Donald G McNeil; New York Times; pages D1 and D6; October 18th, 2011].
Pepin claimed that his exhaustive researches in archives and medical libraries had led him to a mysterious disease syndrome called the “Cachexia of Mayombe”, which, he claimed, might have been an early local outbreak of AIDS in Africa. He wrote that this condition had originally been reported by a French military doctor called Léon Pales, and that it had allegedly killed 50 railway workers on the Chemin de Fer Congo Ocean (CFCO) railway that was built from Brazzaville to Pointe Noire in Congo Brazzaville in the 1920s and 1930s. (Congo Brazzaville was then known as Moyen-Congo, and was one of the territories that made up the sprawling French colony of Afrique Equatoriale Francaise.)
Cachexia is a condition of wasting and general malaise, usually caused by serious illnesses such as cancer. If this was in fact an early outbreak of AIDS, as Pepin suggests, such an event would of course offer huge support to the bushmeat hypothesis. (However, it would not destroy the OPV hypothesis, for it would then have to be established whether these infections represented an early flowering of the present AIDS pandemic, or a dead-end outbreak.) This was clearly an important claim, and I therefore set about locating the 1930s articles and dissertation that Pepin cites.
One of the fundamental faults in Pepin’s book is that it follows a recent regrettable trend in footnoting, whereby endnote indictors are positioned at the ends of paragraphs, rather than at the correct places in the text. This is lazy and entirely unnecessary, but it allows the author to get away with all sorts of imprecision. In the few cases that I have followed up, I have already found several mistakes in Pepin’s book, including examples where the alleged footnote does not support the information it claims to support.
One such example of false endnoting involves the three sources he cites for “Cachexia of Mayombe”. I soon discovered that only the third of these [Revue de la Tuberculose; 1938; 4; 190-208 (the pages are incorrectly cited as 190-198 in Pepin’s book)] was actually relevant. A doctoral thesis about tuberculosis by Jean Auclert, an assistant of Pales, which allegedly contained “more detailed information” is also referenced by Pepin. It took me some time to get hold of a copy, but I finally succeeded a few weeks ago.
The crucial claim made by Pepin is that Pales reported 50 cachetic cases from Mayombe, of which he says that 26 suffered profound weight loss and chronic non-bloody diarrhoea, but with no causative agent being found. However, this is simply incorrect. The original article by Pales clearly states on page 194 that 5 out of 7 of the 26 cachetics who were tested proved to be positive for Shigella, perhaps the best-known strain of dysentery, and an enteropathic organism that is not one of the recognised opportunistic invaders of AIDS.
Moreover, and even more importantly, Pepin states that “severe malnutrition was unlikely” among the cachetics, whereas a page towards the end of the article by Pales in Revue de la Tuberculose strongly suggests exactly the opposite. Here, Pales observes in some detail that most of these railway workers had “been transplanted” from the savanna areas to the north of Mayombe, and from a diet based on millet to one based on manioc (or cassava, a food notoriously lacking in protein), and that this had been done “without a prolonged period of adaptation”. The fact that these men had been press-ganged into service on a particularly difficult section of the railway, where it cut through the tropical forest of Mayombe, and that they had come from other more agriculturally productive regions of AEF strongly suggested that stress, depression and poor living conditions had exacerbated the consequences of a wholly inadequate diet, leading to acute malnutrition and a heightened susceptibility to virulent pathogens such as Shigella.
The individual case histories in the Auclert thesis that Pepin cites make it crystal clear. 22 of the 26 CFCO workers listed here were diagnosed with Cachexie du Mayombe, and 21 of these came from ethnic groups (notably the Gbaya, Banda and Sara) living in the fertile lowland plains of what are now called Central African Republic and Chad. In these lands wheat, maize, sorghum and millet are the staple foods. Check the comparative nutrition tables at the end of the article on “Millet” in Wikipedia. Millet and sorghum have eight times as much protein as cassava by unit weight, and wheat has sixteen times as much.
In short, the Mayombe cachetics were being carelessly worked and starved to death, rather than dying from ancient AIDS.
Interestingly, the passage about the enforced cassava-based diet appears on p. 202 of the 1938 article by Pales, which Pepin does not include as one of the pages in his faulty citation of that article.
While locating these articles in the library, I also came across another article by Léon Pales, one that is not mentioned by Pepin, although it is cited in the Revue de la Tuberculose article: [Pales & Monglond; “Le taux de la glycemie chez le noir en A.E.F.”; La Presse Medicale (Paris); 1934; 38; 765-768]. This article proposes that some of the cachetic workers on the CFCO railway might have been victims of hypoglycemia, suffering from dramatically low blood sugar and diabetes. Hypoglycemia is a serious condition that is often caused by extreme malnutrition or “prolonged starvation”.
The potential impact of malnutrition and dietary imbalance is understood much better nowadays than it was in the 1930s, which means that Léon Pales’ failure to make more of the dietary issue in his attempts to explain the many cases of cachexia is perhaps understandable. Furthermore, the appalling treatment accorded to the railway workers would have been less remarkable in the 1930s than it is today. It is worth noting that in the early 1950s Pales re-examined some of these questions in a further article about the causes of malnutrition; (“Race et Nutrition”, L. Pales; Semaines des hopitaux de Paris; 1952; 28; 706-713).
By contrast, Pepin’s failure to comment on what is happening is inexplicable. If he is any sort of physician, he should surely have recognised that these men were being worked and starved to death.
Moreover, I myself can add the information that among old African hands, including some doctors who worked in Africa in colonial times, the fatalities among CFCO workers in the twenties and thirties have long been rumoured to be examples of “deaths caused by lousy working conditions”.
Since writing the above, I have learnt from further research that there was a vigorous debate about the treatment of the CFCO railway workers led in the late 1920s by the eminent writer, André Gide, and later on by a respected journalist, Albert Londres, who claimed that the local administration had sacrificed the lives of 17,000 Africans. Londres said that the AEF government had fulfilled its promise to bring in workers to build the railway, but “had totally failed to supply transportation, lodging, medical care and food for them”. [Virginia Thompson and Richard Adloff, “The Emerging Sates of French Equatorial Africa”, Stanford UP, 1960, pp 18-19.] Thompson and Adloff imply that working conditions improved in the 1930s, but the evidence from Pales clearly indicates that they did not improve enough.
However, “Cachexie du Mayombe” is a sexy-sounding phrase, and it represents Jacques Pepin’s key argument (indeed, his only argument) to support the idea that there was an early outbreak of AIDS in this area of Afrique Equatoriale Francaise – one that occurred before the recognised pandemic, and before the OPV campaigns of the 1950s. Pepin gets part of the explanation right. Where he’s wrong is in failing to notice that SIV/HIV is neither indicated, nor required, as part of the equation.
So why haven’t other people picked up these anomalies in Pepin’s book? Where are the world-famous fact-checkers of the New York Times? Why do we have reviews by well-known scientists such as Peter Piot (the fomer head of UNAIDS), Robin Weiss, David Mabey and Oliver Pybus, all saying how plausible they think Pepin’s thesis is? Just what is going on here?
The overall impression given by Pepin’s book is that much of it (notably the part about how HIV may have taken off in the African environment of the 1960s and 1970s) is well-researched and that this part represents an honourable contribution to the debate on how AIDS became established in Africa. It is therefore all the more regrettable that the section on the actual origin of AIDS is so shoddily researched and written. Indeed, it is hard to conclude that the mistakes and omissions featured in Pepin’s coverage of the topic of origins are accidental, or have been made in good faith. The “Cachexia of Mayombe” section, in particular, raises significant questions about Pepin’s competence and integrity.
I have recently learnt through the grapevine that a young member of one of the five or six departments which have been actively supporting the phylogenetic dating of HIV-1 and the bushmeat hypothesis did indeed “sort of collaborate” with Pepin during the writing of the book. This man apparently acted as an advisor, which is exactly what I had surmised when reading the book: that someone had been steering Pepin (who, to his credit, is a beautifully fluent writer) in certain directions. He served the advisory role that Craig Timberg admits for Daniel Halperin (with Hahn and Worobey in the wings) in Tinderbox. This same advisor is also featured on the back cover of the Pepin book, singing its praises.
I believe, in short, that Jacques Pepin may well have been co-opted by the bushmeat theorists, with his book, sadly, becoming part and parcel of the continued cover-up on this subject organised by a number of interested parties.
I suspect that this book (just like Tinderbox) has been placed in the public domain specifically in order to provide a back-story for the supporters of the bushmeat hypothesis, one that can be cited subsequently as “further evidence against the OPV hypothesis”.
Once again we see evidence of a determination by the medical establishment in several Western countries to bolster and support the intellectually flimsy framework of the bushmeat theory.
Within the same context, it is worth noting that huge grants (such as the $5M given by the Gates Foundation to Beatrice Hahn’s group at the University of Alabama) have been awarded to many of the bushmeat proponents in the last few years. Other groups (such as Eddie Holmes’ group in the Department of Biology, Bill Hamilton’s old department at Oxford University) have been awarded new, expensive buildings such as P4 laboratories. Other bushmeat supporters have been significantly promoted, notably Paul Sharp, who in 2007 moved from Nottingham to become a high-profile professor in the Institute of Evolutionary Biology at the University of Edinburgh, and Michael Worobey, formerly from Holmes’ group in Oxford, who in 2003 was suddenly awarded a professorship and his own lab at the University of Arizona (just down the road from Bette Korber at Los Alamos, with whom he had been in intense discussions some months before his appointment).
It should also be noted that Beatrice Hahn has followed in the footsteps of her former boss, Robert Gallo, by taking out private patents on the products of much of the work done in her publicly-funded laboratory. These include patents on the complete genome sequences of different SIVs and key parts of the envelope gene of HIV-1, which might come in useful in the development of an HIV vaccine. Professor Hahn, her husband George Shaw, Paul Sharp and Preston Marx, among others, are referred to as the “inventors”, although how you can be the inventor of the genomic sequence of a virus, I’m not quite sure. (Any who are interested can check the Google Patents web-site link for Beatrice H. Hahn.)
It would appear that being a bushmeat origin supporter does not do too much harm to your career prospects, or, for that matter, to your bank balance. On this, at least, Michael Worobey appears to have been speaking the truth!
Footnote: * (0.8 – 2.4 people) times 1.89% = (0.015 – 0.045 people) = “1/67 to 1/22 of a person”.
Edward Hooper. April 25th, 2012.