The Bushmeat Gang (The Gang That Couldn’t Tell The Time!)

[This is a response to Worobey et al.: “Island Biogeography Reveals the Deep History of SIV” (Science; 2010; 329; 1487), and to the related article by Donald G. McNeil Jr. in the New York Times, “Precursor to HIV was in Monkeys for Milenniums” (NY Times; September 16, 2010).]

The Donald McNeil article in the New York Times invited comments from the public, and in the following 24 hours 101 comments were logged before the Comments section on this topic on the Times web-site was closed.

As author of “The River: A Journey To The Source of HIV and AIDS” (Little, Brown; 2000), a book that strongly favours the hypothesis that AIDS is iatrogenic [and the oral polio vaccine OPV) theory of origin of AIDS], I was immensely pleased to realise that 20 of these 101 comments alluded directly or indirectly to “The River”, to myself as author, to the OPV theory, to the film made about that theory (“The Origins of AIDS”), or to some combination of the above.

Whereas many of the comments made about Worobey’s SIV paper were highly critical, all 20 comments about the OPV theory were favourable, some extremely so. Many of them pointed out the effort that had been put into trying to suppress the theory and to discredit me. The public, it seems, it not as easily fooled as certain scientists like to believe.

The Bushmeat Gang is so called because they apparently believe that the AIDS pandemic began after an African became infected with the ancestral virus to HIV-1 while he or she was eating, or cutting up, chimpanzee bushmeat. I would like to add a few comments of my own to this latest research by Michael Worobey and other members of The Bushmeat Gang about the age of SIV.

1) Worobey et al. are to be commended for recognising that SIV, the simian counterpart of HIV, is much older than they and their molecular biologist colleagues had previously thought. In fact, this latest paper in Science is considerably more helpful than many of their recent articles about HIV and SIV, almost all of which have involved attempts to date HIV by genetic methods, by means of a so-called “molecular clock”. This may well be because of the involvement as last author of Preston Marx, the virologist from Tulane National Primate Research Center in Covington LA (previously Delta Primate Research Center), who despite being a de facto member of The Bushmeat Gang, still has a decent working brain in his head. The article is
based on a single clear premise: that it might be beneficial to examine the primates living on Bioko (the island formerly known as Fernando Po, lying just off the west coast of Africa), to see if any of them carried SIVs that could be compared to SIVs found in the same species living on the African mainland. (Unless the Bioko primates had been brought to the island by sailors, it seemed reasonable to propose that the island and mainland primates – and their SIVs – might have been evolving separately since the two places were last joined by a land-bridge, which apparently was presumed to be at least 10,000 years ago.) SIVs were found in the drill (a large baboon-like primate) on both Bioko and the mainland, and a comparison of these two viruses suggested to Worobey and his team that the two SIVs had been evolving separately for almost 77,000 years (a range of 33,000 to 133,000 years).

This in turn suggested that SIV in general might be a much older virus than the molecular daters had previously hypothesised, and clearly caused many of them some surprise. Worobey closed by suggesting that it “may be worth investigating” whether HIV as well might be older than previously thought.

2) However, comments such as this latter one by Worobey are all based on the erroneous concept that it is possible to date the ages of immunodeficiency viruses by genetic methods, as if the evolution of these viruses occurs at a constant rate, like the regular ticking of a “molecular clock”. Research published 7 years ago by Wain-Hobson and Meyerhans (J. Gen. Virology; 2003; 84; 885-895) showed that the”recombination rate of [HIV] exceeds the point mutation rate by a factor of 10″. In other words, 90% of the evolution of the HIVs occurs through recombination and not through mutation. Yet the molecular clock model measures only mutation; it is incapable of measuring recombination. Ignoring this, geneticists like Worobey and Hahn continue to use a variety of arguments in order to try to salvage their flawed model. They use what they like to call a “relaxed molecular clock” (presumably meaning a clock that does not tick regularly, which seems to me a very useless sort of clock). They also claim that they exclude recombinant sequences from their datasets before they begin their calculations. (In reality it is impossible to do this, because recombination that occurs near the beginning of the evolutionary history of a virus cannot be identified today. Therefore many of the viral sequences that they use for their calculations are unrecognised recombinant viruses, and this irrevocably slants their results.) Put simply, Worobey and Hahn and the Bushmeat Gang can’t help themselves; they can’t resist. It is so damned easy to calculate ages for the HIVs using their methods that they end up doing it again and again, even when it’s clear that the model on which they are basing their calculations is inherently flawed. Whether they realise it or not, their results only confirm their own preconceptions and prejudices. Their work thus becomes an exercise in self-fulfilment, a naked emperor inviting the court to applaud his taste in clothes. I receive many emails from scientists and others who clearly recognise that their research is intrinsically flawed, but the great majority insist that they should not be quoted. The origin of AIDS is a hugely loaded issue, one that is recognised as having the capacity to end scientific careers.

3) My own position on this latest paper is to concur with the comments of Preston Marx. SIV is so widely dispersed across Africa that common sense alone suggests that the virus must have been present on the continent for at least several tens of thousands of years. Recent phylogenetic dating papers suggesting an SIV age of only a couple of thousand years have clearly been erroneous. So I would not take issue
very much with the age of SIV that Worobey et al. propose, in that common-sense suggests that in this instance their estimate may not be way out. What I would take issue with, however, are their methods of
calculating that age. Using a molecular clock is a good way of dating the age of a normal (DNA-based) virus like yellow fever or smallpox that evolves almost exclusively through mutation, but it does not work
well for retroviruses, and in particular for the most mutable (or recombinogenic) retrovirus of all, HIV. Although it is not proven what percentage of the evolution of the SIVs occurs through recombination, SIVs are also retroviruses and so, like the HIVs, they are also highly prone to recombination. In commenting on these results in McNeil’s article, Hahn admits that previous methods of dating SIV which concluded that the virus was merely a few hundred to 2,000 years old “just didn’t seem right”. Now, however, the molecular daters are in a quandary. As they admit in the Bioko article, they now have to try to explain why HIV apparently evolves 125 times faster than SIV! Worobey even proposes that maybe they should look again at the HIVs, to see if they might be older too. Here he ignores the simple and obvious fact that I recall Preston Marx and myself discussing together back in 1995: the total lack of evidence of HIVs being brought across to the United States and the Caribbean by the 12 million or more slaves involved in the Slave Trade of the seventeenth to nineteenth centuries. Save for isolated hangovers, the Slave Trade effectively ended in the 1860s, which indicates that HIV must be less than 150 years old. (But there again perhaps Worobey and Hahn hope to find an ancient HIV in the corpse of a slave from the early 1800s. One worries at the potential for malfeasance here.)

4) Why are so many apparently reputable scientists touting this nonsense? Well, perhaps it is because touting such nonsense does seem to lead fairly directly to fortune and fame. One of the scientists
involved (Worobey) has, at an unusually young age, been awarded his own lab in which to pursue these studies, while another (Hahn) has been awarded a huge ($5 million) grant to assist her researches. The
latter grant came from the Gates Foundation rather than the US government, and we all applaud Bill Gates’ philanthropic instincts. However, one must also bear in mind that Gates is still chairman of a massive
corporation (Microsoft) that is beholden to the US government in all sorts of ways. Would it be wise to bite the hand that feeds? It is noteworthy that another (wholly laudable) aim of the Gates Foundation is to complete the eradication of poliomyelitis from the planet, a goal that was initially scheduled for Year 2000. Many of those who are most vociferous in support of the molecular dating work of Worobey and Hahn, such as the people who produced the oral polio vaccine that was field-tested in Africa in the late 1950s (doctors Koprowski and Plotkin) have noisily claimed that the reason why the polio eradication programme failed was because of the effect of my book “The River” on populations in Africa where polio is still endemic; they falsely claim that my book has persuaded Africans not to take polio vaccine. Stanley Plotkin, in a particularly odious outburst, even went so far as to blame me personally for every further death that occurs from polio, an interesting accusation coming from a man who started his career at Koprowski’s Wistar Institute attending meetings at Fort Detrick where he gave advice to America’s leading military experts in biological warfare! But not for the first time, the “facts” claimed by Koprowski and Plotkin are not facts at all, but merely fabrications. Africans from many countries have been suspicious of vaccines since they were first introduced in the late nineteenth century. Sometimes this has been with good reason, for several of the early vaccines were in some way flawed. The reasons given by the African vaccine refusers vary, but the most frequently quoted reasons in the last 30 years include claims that the vaccines contain anti-fertility drugs, “cancer”, or “AIDS” (the disease, rather than HIV). Koprowski’s reference to an article in a Kenyan newspaper that claimed to prove that polio vaccine refusal in Kenya was caused by “The River” featured an incorrect reference, and the article he alluded to (which I found by searching through newspaper clippings files in Nairobi) did not say what he claimed it did. The reasons for peoples in northern Nigeria refusing to take current polio vaccines in the last few years are complicated, but Nigerians whom I have consulted about this matter assure me that they relate to political and religious differences between the Christian and Islamic parts of that country, rather than to any knowledge of my book.

5) Bushmeat Gang members such as Beatrice Hahn, Paul Sharp and Michael Worobey, neglect to address the counter-evidence that stands in front of them like an African elephant. Let me try to summarise that

a) The weakness of the molecular clock model. Their rates of evolution for SIVs and HIVs now differ by a factor of 125. Worobey asks rhetorically whether they should perhaps further back-date their
calculations about the age of HIV-1, (presumably in an attempt to lessen the differences in the evolutionary rates). How casually they present their hypothesised dates – dates that, in interview, they often refer to as if they were proven facts. But don’t these massive discrepancies ever suggest to them that there might be something fundamentally wrong with their research?

b) The weakness of their interpretations of the evidence. The earliest proven sample of HIV-1 comes from the Belgian Congo capital of Leopoldville; it dates from 1959, and it was first identified as
HIV-1 in 1985. Despite 25 years of further searching, nobody has since found an earlier sample of HIV-1. Two years ago, Worobey announced the discovery of a further sample of HIV-1 dating from 1960, which also allegedly came from Leopoldville. Worobey’s conclusion? That the two viruses (from 1959 and 1960) differed genetically by 12%, and that by “backdating the molecular clock”, he could demonstrate that HIV-1 dated back not to 1931, as his colleagues had previously claimed, but all the way back to 1908. Because his molecular clock model does not allow for it, he completely ignores the far more plausible conclusion that some event in Leopoldville that occurred shortly before 1959 might have had relevance to the first two appearances of pandemic HIV-1 on the planet, which came one year apart – and 16 years before the next appearance (in 1976, also in a woman who had lived in Leo). CHAT polio vaccine was first tested in Leopoldville in August 1958; between then and April 1960 it was given to all 75,000 of the city’s children aged up to 5 years. The 1959 infectee was a male, but we know nothing of his age, even though he was officially classified as an “adult”. (My research has revealed that some of those who gave blood in these tests, though listed as
“adults”, were actually as young as 3 years.) The 1960 HIV-1 sample allegedly came from a 23-year-old woman, who was obviously not one of the children vaccinated with CHAT. However, it should be noted that
at least as early as February 1957 CHAT had been tested on other very mobile groups (including at least 12,000 soldiers and soldiers’ families from the Force Publique, the Congolese army) who at that time were based in towns in the eastern part of the Belgian Congo. In those days Force Publique soldiers changed camps every six months, which (according to my calculations) means that by early 1959 approximately 1,000 of these 12,000 vaccinees should have been living in the main army camp in Leopoldville, and that well over 1,000 vaccinees would have passed through there in the intervening period. Why is this relevant? (a) Because, as readers of this site will know, I have been arguing for some time (on the basis of multiply-confirmed historical researches) that some of the batches of CHAT vaccine that were administered in the Belgian Congo had been grown locally (in the Congo) in chimpanzee cells, and that after recombination between different chimp SIVs took place in the tissue cultures used to prepare the vaccines, different HIV-1 variants were transferred to the vaccinees in some of these vaccination campaigns. And (b) because this means that although adult Africans were not officially vaccinated with CHAT in Leopoldville, the 1960 HIV-1 infectee may well have been a CHAT vaccinee from another town.

c) The inbuilt bias to their phylogenetic analysis. When I travelled to Nottingham in 1994 to discuss these issues with one of the molecular biologists involved, Paul Sharp, he strongly advised me to go and consult his colleague, Beatrice Hahn. The next year I did so. I travelled to Birmingham, Alabama to speak with Hahn, but unfortunately she was not willing to listen to what I had to say for longer than sixty seconds. She was so convinced by the merits of her own research that she simply talked over my presentation in order to tell me about her own research. I was in the early days of this investigation, and at that stage was not confident enough to insist that she listen to my plausible alternative hypothesis – one that, even in those days, appeared at least as logically tenable as her own. For what it’s worth, my own belief is that Beatrice Hahn and Michael Worobey may not be knowingly participating in the cover-up that has been staged by the doctors who fed CHAT vaccine in the Congo in the 1950s. But their ambition, and eagerness to profit from their clearly flawed “molecular dating of HIV” claims has led to their becoming conspicuous allies of the CHAT vaccinators. My own impression of Beatrice Hahn, an impression that others, including some who have worked in her lab, have substantially reinforced, is of a determined, intelligent and hard-working scientist, but one who is signally lacking in wisdom. She is so obsessed by her own hypotheses (and the exciting possibilities that she believes they engender) that she is unable to countenance possible alternative views – and that arrogance is her fatal flaw as a scientist. In the past, when commenting on Michael Worobey’s 1908 paper (Nature; 2008; 455; 661-664), Hahn stated baldly that: “In HIV, genetic difference equals time”, an innocent-sounding equation which demands a complete ignoring of the limitations of the molecular dating approach for retroviruses, and an ignoring also of the historical evidence of OPV use in the Congo; [“HIV Virus Took Hold in Humans 100 Years Ago, in Africa’s Colonial Cities”; Discover; 1st October 2008]. According to the same article, Hahn translated this “genetic difference equals time” assertion into the equally unsupported assumption that by 1960, HIV-1 must have already infected “a few thousand Africans”. Let us recap to see how she arrived at that amazing conclusion. She (and Sharp and Worobey) believe that the index virus crossed into humans somewhere in south-eastern Cameroon in or around 1908, and then travelled 500 miles down two river systems to Leopoldville, where it existed for 50-odd years, quietly infecting “thousands” of people. By contrast, the alleged early focus of infection seems to have died out entirely in south-eastern Cameroon.What she therefore has to assume is that AIDS cases were occurring in Leopoldville throughout the first half of the twentieth century, but went unrecognised by the doctors working there. But if you ask any physician who worked in Leopoldville, or indeed the Congo, during the period up to 1960 (and I have interviewed many), they will tell you this is simply not the case. Had there been cases of an AIDS-like disease syndrome in those colonial days, they would have recognised these cases as something new and alarming, and recorded them for posterity, perhaps as “interesting diseases of unknown origin”. Let me state clearly: I am not a scientist, but I am a careful medical researcher, and I have spent over 20 years working on this topic. The colonial archives and journals of tropical medicine do not record any plausible cases of AIDS until 1962, when a woman originating from Lisala (a site of early CHAT vaccination, probably in 1957 or 1958) died in Leopoldville/Kinshasa with massive, disseminated Kaposi’s sarcoma (KS), pneumonia, and multiple untreatable bacterial infections. Writing retrospectively in 1987, the reporting doctors, led by the great Belgian physician Jean Sonnet (Scand. J. Inf. Dis.; 1987; 19; 511-517), drew a clear distinction between the 1962 case and another case of disseminated and visceral KS that they had seen in Leopoldville in 1960, in which the clinical presentation (indolent course; lack of any other opportunistic infections) was very different. (Acta Clinica Belgica; 1961; 41; 313-331). Later, speaking to me in the 1990s, both of the two principal authors of this report told me that the 1960 case had almost certainly not been caused by HIV, whereas the 1962 case surely had been. Similarly, the first three cryptococcosis cases reported in the Congo (in the early 1950s, before the polio vaccine campaigns) are very unlikely to have been HIV-related, not least because they lacked any other of the concomitant opportunistic infections that are typical of AIDS. All three patients went untreated with antibiotics and all three died, but when three further cryptococcosis patients were treated by Jean Sonnet’s team with the newly-available antibiotic, amphotericin-B, in 1960-1962, all three quickly recovered. (Ann. Soc. Belge Med. Trop.; 1963; 43; 751-776.) By contrast in the 1970s there was a spate of reports from Kinshasa and elsewhere in the Congo of untreatable cryptococcosis, KS and tuberculosis, often combined with other diseases, and it is this that demonstrates the start of the AIDS epidemic proper (an epidemic that would soon become a pandemic). What all this reveals is that Sonnet’s 1962 AIDS case was exceptional for the 1960s, and that it stood out like a sore thumb. If Hahn’s statement about a “few thousand Africans” being infected in 1960 had been correct, then AIDS would certainly have been recognised in Leopoldville in the 30s or 40s, and certainly long before 1962 (by which time doctors would surely have been reporting dozens of AIDS cases). For researchers like Hahn and Sharp and Worobey to argue (or imply) that 1000s of Africans were infected with HIV by the end of the 1950s suggests that although they are hugely experienced in their own particular fields, they are insufficiently rigorous in their analysis, and that they lack that important human quality – basic common sense. For what it’s worth, my own theory – which is based on the earliest observed instances of HIV-1 infection and AIDS – is that by 1960 there were between ten and a few dozen people infected by HIV-1. I believe that these were not links in a chain of human infection affecting “thousands” of people and stretching back 50 years, but rather some of the first few unfortunate infectees with a recombined chimpanzee SIV that had contaminated different batches of a live vaccine grown in chimpanzee cells, and administered to hundreds of thousands of Africans in the last three years of the 1950s. Only a small proportion of those vaccinees (including those who were already immuno-compromised, or who had cuts in their mouths or bleeding gums) would have become infected by the chimpanzee SIV that contaminated the vaccine, and it is these persons who became the index infectees with the different clades of HIV-1(M) that are now called subtype A, subtype C and so on. The 12% genetic difference that Worobey observed between the 1959 and 1960 HIV-1 sequences does not represent 50 years of HIV-1 evolution, but rather the difference between two viral variants, the index cases of two clades of HIV-1, emerging from two different soups of recombined chimpanzee SIVs. Of course, there is no way for a molecular clock to be able to model an iatrogenic catastrophe such as that one. All a molecular clock can do in this instance is to fabricate a false prehistory for HIV, one that consciously or unconsciously fits with the preconceptions of the scientists calibrating the clock.

d) Inaccurate claims about the chimpanzee sub-species present at Lindi Camp. Hahn argues that the chimpanzees that carry the SIV that is directly ancestral to pandemic HIV-1 come not from the Belgian Congo, now called the Democratic Republic of Congo or DRC (where the main common chimpanzee sub-species is Pan troglodytes schweinfurthii), but those from south-eastern Cameroon, where a different sub-species of chimpanzee, Pan troglodytes troglodytes, is found. I don’t agree with her that the sub-species is necessarily crucial, for the evidence from the mammalian phylogenetic tree suggests that the individual members of those two alleged sub-species are intertwined, and that they therefore may in fact represent just a single sub-species. [See Gagneux et al., Phil. Trans. Roy. Soc. (London) B; 2001; 356; 889-900.] But more importantly, I have provided documentary evidence showing that at least one Pan troglodytes troglodytes chimp was present at Lindi camp in 1959-60. (At Lindi, animals were co-caged and group-caged together, thus allowing onward transmission of viruses.) In past essays, I have also reported further evidence which suggests that several Pan troglodytes troglodytes chimps may have been present from an early stage at Lindi Camp (which opened in July 1956). There are in addition two further pieces of evidence which I am holding back for now, both of which strongly counter the claims by Worobey and Hahn that they have disproved the OPV theory on the basis that the chimpanzees of Lindi camp were “the wrong chimpanzee”. These wiill be published when the time is right.

e) The dearth of convincing new HIV infections. Unfortunately for Hahn and Worobey and The Bushmeat Gang, the evidence that they need to support their theory of HIV being 100 years old is strangely lacking. Given the increase in bushmeat consumption across Africa, and given how closely they are monitoring the situation, especially in a country like Cameroon where they claim the crucial SIV transfer to humans occurred, they should be finding evidence of ever-increasing SIV transfers from African primate to human. Unfortunately, such evidence seems to be minimal. The Hahns like to claim that there have been at least nine transfers of primate SIV to humans in Africa. This is misleading, because what they fail to point out is that most of these represent instances of single human infections. In all likelihood, therefore, these are examples of a “dead-end infections” – namely an SIV infection that has been acquired by an African from an African primate, but which is apparently not transmissible from person to person. But one thing worth noting here is that the rules agreed upon by these same geneticists state that you need at least 3 examples of a strain before you can name something as a distinct genetic group or clade, such as HIV-1(M). But when it suits them, it seems, they forget their own rules, and a single infectee is enough. A good example of the “single-infectee HIVs” is the allegedly new HIV-1(P) strain, allegedly found in a 62-year-old Cameroonian woman living in France, and announced in August 2008. In that article it was claimed that HIV-1(P) was “closely related to” SIVgor, a new type of SIV that had apparently been found in three Cameroonian gorillas, a finding initially announced in November 2006. (Most people believe that SIVgor represents a chimp virus that has crossed recently to gorillas, but let’s leave that for now.) The Cameroonian HIV-1(P) infectee was apparently identified in 2004, when her serum was sent to a national reference centre lab in Rouen, northern France, run by Dr Jean-Christophe Plantier; the virus gave indeterminate results, and so he sequenced it in 2005, discovering the unusual virus. I emailed Dr Plantier for further details, and some weeks later he sent a very pleasant and helpful reply. He was unable to provide very much additional information about the infected patient, apart from confirming that she had reported no contact with apes or bushmeat, and that her infection had therefore, he felt, probably been acquired sexually. But he did reveal an intriguing detail that had not come out in the scientific articles or in the press: that he was a former assistant to, and remains a close collaborator of, Professor Francois Simon. [This is the same Professor Simon who for many years headed the Franceville primate centre in Gabon, which is the major primate centre in Francophone Africa, in existence since colonial times. Professor Simon is also the researcher who discovered HIV-1(N) – see below – in the early 1990s.] Apparently Plantier was Simon’s assistant when the latter worked at Rouen hospital (presumably also in the national reference centre) from 2000 to 2003; the two collaborated on work involving centres in Cameroon and Gabon, including an important paper out of Franceville in which two different strains of SIV were reported in a mandrill. (J. Virol.; 2001; 75(15); 7086-7096). It is admirable that the French should have put in place a system for picking up unusual variants of HIV. However, it is remarkable that a human infection with HIV-1(P) should have come to light at almost the same time that the same band of researchers were discovering the “closely related” virus, SIVgor. It is also worth noting that research published this week in Nature reveals that gorillas (rather than chimpanzees, as had been posited in 2009) are the likely source of the most severe strain of human malaria, Plasmodium falciparum; (Nature; 2010; 467;420-424; see also 404-405 for commentary by Holmes). The latter research is fascinating, but it should be noted that SIV (spread by blood and sex – and iatrogenically via one particular vaccine) is very different from malaria, which is spread aerially via a mosquito vector. Or are the bushmeat people in so desperate a bind with their “AIDS started in south-east Cameroon” theory that they plan to propose that pandemic HIV [and not just the very rare HIV-1(P)] originated from gorillas, rather than chimps? If so, then the arguments could get really interesting! (My guess is that they will be content to imply the possibility, and leave it at that.)

f) The Bushmeat Gang’s ignoring of other viable explanations for the SIV outbreaks in humans. What Hahn also fails to point out is that only four of these nine or ten alleged transfers of SIV from African primate to human [(HIV-1(M), HIV-1(O); HIV-2(A) and HIV-2(B)] have caused large outbreaks or epidemics of HIV. In each of these four instances, the earliest evidence of human infection dates from the 1950s or 1960s, just years after the experimental polio vaccine trials were conducted. (Such trials were conducted not only in the Belgian Congo, but also in the French colonial territories of French West Africa and French Equatorial Africa, starting in 1957. [See the revised Postscript to “The River”, paperback edition (2000); pages 827-877.] These are exactly the places where the other large outbreaks of HIV infection occurred, in addition to the Belgian Congo.) There has been just one other HIV outbreak, that of HIV-1(N), of which only six human infectees have been discovered, all in the 1990s. However, there have been no further HIV-1(N) infectees found in the last decade, so it seems that this strain may well have died out. HIV-1(N) may possibly have been an instance of bushmeat-derived HIV, although equally it could have been a late-revealed example of vaccine-derived HIV. I am perfectly prepared to accept that bushmeat transfers of SIV to humans may occasionally happen. It’s just that it is not these, it seems, which spark major outbreaks of HIV and AIDS. Major outbreaks of HIV infection seem rather to be linked to iatrogenic events, in particular to the use of SIV-infected primate cells for experimental polio vaccines that were tested on large numbers of Africans (probably more than one million in total) in the middle of the twentieth century, just prior to Independence.

g) The apparent disappearance or non-reporting of important samples. Over the last 6 or 7 years, Hahn’s group has been collecting hundreds of samples of chimp urine and faeces from the former Belgian Congo (now called the DRC, the Democratic Republic of Congo), but they have revealed nothing of their results. (I have reliable information, however, indicating that many of these samples have turned out to be SIV-infected.) Similarly Michael Worobey has, since 2001, had samples of the pathology slides and paraffin blocks from the basement of the Laboratoire Medical de Stanleyville (LMS), which might well have revealed early traces of HIV, yet he has announced nothing about the testing of those samples. His group apparently managed to obtain the rest of the ancient LMS samples in or around 2005 or 2006, courtesy of Jean-Jacques Muyembe, a leading Congolese virologist from Kinshasa (formerly Leopoldville). Muyembe went up to Kisangani (formerly Stanleyville), both to obtain the rest of the LMS samples, and to interview people from the LMS and Lindi Camp. There is concrete evidence that after speaking with Muyembe, at least one Lindi witness changed his account (in this instance with regard to the date when he began working in the LMS virology lab, a crucial historical detail). Sadly Muyembe and his bosses, we had already filmed this witness in 2001, and had also filmed his identity card, showing when he began working there. In short, it seems that Dr Muyembe was engaged in a cover-up – in this instance pressuring some of my former witnesses into changing key details of their stories.

It is a desperate shame that molecular research into African HIVs and SIVs is now almost completely dominated by highly ambitious people like Worobey and Hahn (and their collaborators such as Muyembe), because their way of doing science seems to be highly questionable and partisan. They publish data when they feel it lends support to their theories, but they apparently suppress evidence that works against them. This is a huge claim I am making, but it does need to be made. These members of The Bushmeat Gang are not merely incapable of telling the time properly. They are also not impartial scientists.

If the OPV theory were ever to be disproved, I believe that I would have the integrity to make a public announcement that I had been wrong, and – at the very least – apologise. However, I don’t for one second think that I will ever have to do that, because the OPV theory is supported by a fabulously rich fossil record – a record that also reveals much of the cover-up that has been staged to protect the CHAT vaccinators.

But the question that keeps occurring to me is this. What will the Bushmeat Gang and the CHAT vaccinators do when their theories are proved wrong, as they surely will be? Will a single one of them be prepared to accept responsibility for having made a dreadful error, one that has retarded HIV research by more than a decade?

Ed Hooper Originally written 23rd September 2010; updated 22nd October and 20th November 2010.