As forecast in my piece ‘Worobey’s wobbly research’, first posted on this site on March 19th, 2008, the Canadian molecular biologist Michael Worobey has just published new calculations about the age of the AIDS virus, HIV-1, which place its origins even further back in time.
His work appears in the form of a lengthy letter to the journal Nature, entitled ‘Direct evidence of extensive diversity of HIV-1 in Kinshasa by 1960’, by M. Worobey, D.E. Teuwen, M. Bunce, S.M. Wolinsky et al.; [Nature; 2008 (October 2nd); 455; 661-664.]
On the basis of this one newly-discovered sample of HIV-1 dating from 1960, Worobey and his colleagues contend that the first human infection with the AIDS virus occurred in 1908, with outer confidence limits stretching from 1884 to 1924.
The previous ‘best guess’ of molecular biologists such as Bette Korber was that the first HIV-1 virus existed in a human being by 1931. This in itself was a highly dubious finding. But the 1908 ‘guestimate’ by Worobey and his team from the Department of Ecology and Evolutionary Biology at the University of Arizona is now being highlighted by extensive coverage and publicity in Nature, and then spoon-fed to a largely compliant press corps.
Worobey’s calculations, according to his supporters Beatrice Hahn and Paul Sharp, who have been invited by Nature to write the accompanying commentary, employ ‘state-of-the-art statistical analyses’. But they are actually based on just the one crucial new piece of data, this being a fragment of genetic sequence allegedly obtained from the stored lymph node of an African woman in 1960. Just like the the famous 1959 sample (the oldest known sample of HIV), this 1960 sample comes from a subject who was then living in the Belgian Congo capital of Leopoldville, (now Kinshasa, Democratic Republic of Congo). This, quite clearly, is a significant detail, and yet not one of the press articles covering Worobey’s paper seems to have picked it up. I, and the small group of people on whose wisdom and scientific expertise I informally rely (three quarters of whom are professional scientists, some of them quite eminent scientists) are strongly persuaded that these exciting-sounding dates from Worobey are highly dubious. We believe that his analysis and interpretation of the 1960 viral sequence are in reality little more than wishful thinking based on poorly-supported science.
We also believe that the discovery of that 1960 sample of HIV-1, and the coincidence of place with the 1959 HIV-1 sample, is the real story here, not Worobey’s highly speculative 1908 guestimate of when the first AIDS virus might have existed. A much simpler and better-supported explanation for the recently- discovered 1960 HIV-1 fragment is that both it and the 1959 HIV-1 fragment are the results of the administering in Leopoldville and elsewhere in the Belgian Congo from 1957 onwards of different batches of an experimental live vaccine. This vaccine, an oral polio vaccine (OPV) called CHAT, was (as I have previously demonstrated) prepared locally in the Congo in chimpanzee cells, which cells were themselves almost certainly contaminated with SIVcpz (chimpanzee SIV, the immediate primate ancestor of HIV-1).
Part 1 of this essay gives a brief background to Worobey’s latest paper.
In Part 2 I provide some analysis of the paper, and attempt to demonstrate where Dr Worobey has gone wrong.
In Part 3 I shall provide a much simpler explanation for the existence of this new HIV-1 sequence from 1960.
In Part 4 I shall provide some historical background to Dr Worobey’s involvement in this debate.
And in Part 5 I shall provide more information about the large organised cover-up that has taken, and is taking place on this issue.
In the 23 years since 1985 (just over a year after scientists had first developed the ability to test for the presence of HIV-1) there has been just one single truly ancient sample of HIV-1 known to scientists. This ancient sample of virus came from a blood specimen initially taken in 1959 from an African male from Leopoldville, in what was then the Belgian Congo. Scientists have searched hard for nearly a quarter of a century, but they have still found no earlier sample of HIV-1 in the entire world. [Originally, in 1985, this sample was described as HIV-positive because it tested positive in a series of antibody studies. Later, in 1998, the viral sequence (ZR59) of HIV-1 fragments obtained from this 1959 sample was published.]
Now, in 2008, the team of Michael Worobey have announced the discovery of another ancient sample. It apparently comes from the stored lymph node of an adult African female, and was taken in 1960. And it was obtained from the very same city, Leopoldville – now called Kinshasa in the Democratic Republic of Congo (DRC).
For perspective, the next earliest known sample of HIV-1 dates from 1976, fully sixteen years later – and it also was taken from a subject in the DRC (one who had worked for some years in Kinshasa as a femme libre, a ‘free woman’who had had several different sexual partners. The often-used translation of ‘prostitute’ is a little too simplistic.)
Members of Michael Worobey’s team have obtained a genetic sequence from the tiny fragments of virus that they have managed to recover from this 1960 sample of HIV-1. (A genetic sequence is a list, in sequence, of the individual nucleotide bases – A, C, G and T – that make up an organism, in this case the HIV-1 virus.) There are questions that could legitimately asked about this sequence, but it is too early to go into details, given that the sequence details have only recently been released to Genbank. I think that for now it is better to leave such concerns aside, and to assume that the 1960 sequence is a genuine sequence.
(2) An analysis of Worobey’s paper, including some observations of where Worobey has gone wrong.
Worobey’s team has gone on to use this genetic sequence from 1960 in an attempt to bolster their ideas about the age of AIDS. Employing their molecular clock hypothesis, they compare their segment of the 1960 sequence with the fraction of genetic sequence that exists from the 1959 HIV-1 virus, and they compare these in turn with other more modern HIV-1 sequences from around the world. Then, assuming that the evolution of HIV takes place at a constant rate, they extrapolate backwards to predict the age of the AIDS pandemic.
They claim that the two HIV-1 viral sequences from 1959 and 1960 are so genetically different one from the other (the difference is actually just under 12%) that this forces back the date of the first HIV-1 virus even earlier in time. In year 2000, the team of Bette Korber at Los Alamos, New Mexico (which is closely allied to the Worobey group in Arizona) proposed that the first HIV-1 had existed back in 1931. But now Worobey and his team propose that this index HIV-1 infection existed in 1908.
The aforesaid molecular biologists and geneticists deal with huge tranches of molecular data, and conduct their work on super-computers. They presume that they can measure the age of HIV-1 through a molecular clock (or phylogenetic clock) that ticks regularly, like a metronome.
However (as several scientists and I myself have been pointing out for more than six years now), the basic assumption that underlies all of their work, that the evolution of HIV-1 occurs at a constant rate, through mutation, is erroneous.
The molecular clock does offer a fairly reliable method for deciphering the past history of most viruses, which are DNA-based, and which do evolve predominantly through mutation. However, HIV is a retrovirus, and is RNA-based – and nine-tenths of HIV’s evolution occurs through recombination, a completely different form of viral evolution. Unfortunately, the molecular clock is unable to measure recombination. HIV-1 is in fact the most recombinogenic virus (the virus most prone to recombination) known to medical science. And this means that the molecular clock, which measures only mutation, is an inappropriate hypothetical model for measuring the evolution of HIV-1.
Yet Worobey and his colleagues (just like other proponents of the bushmeat hypothesis of HIV origin, such as Paul Sharp, Bette Korber and Beatrice Hahn) ignore this simple fact.
They acknowledge that recombination in HIV-1 presents a problem for the dating of HIV-1, but argue that they have taken steps to remedy this. For instance, they say that they have excluded recombinant sequences from the dataset of HIV-1 viruses which they use for their analysis. But in reality they are unable to do this – the main reason being that you cannot identify recombination if it occurs early in the evolutionary history of a virus. Because they cannot recognise all recombinant sequences, they are unable to remove all recombinant sequences from their dataset.
It is interesting to note that what Dr Worobey finds most useful for his analysis (just like doctor Sharp before him) is something he refers to, deliciously, as a ‘relaxed molecular clock’. This means a clock that ticks at a regular rate when they want it to, but which begins to bend time when they need some extra elbow-room with their calculations! Thus it is that Worobey and his team arrive at that HIV-1 start date of 1908. It sounds impressive. But in reality, it is simply a casserole of ambition and wishful thinking. When I used to speak with him back in 2000 to 2002, Michael Worobey used repeatedly to say that because of the impact of recombination, any attempt to date HIV-1 through phylogenetic means ended up as ‘a dog’s dinner’.
Now he has changed. Nowadays he states that the effect of recombination on dating HIV-1 can be ignored. But the work that he cites to support this contention relies on an assumption that recombination only occurs on the ‘terminal branches’ of the phylogenetic tree, which represent the most recent HIV-1 sequences.
But Worobey offers nothing to support this assumption, which (as I demonstrate below) is inherently unsafe. What Professor Worobey has done, in effect, is to brush the whole issue of recombination under the carpet.
Let me explain in rather more detail why I dispute the findings of Michael Worobey, and of these eminent geneticists and molecular biologists who support him.
Essentially, Worobey and his friends are wedded to two preconceptions. These are:
(a) that one can date the age of HIV-1 (a virus which evolves mainly through recombination) by means of a molecular clock (a theoretical device which cannot allow for recombination, and which only measures evolution through mutation); and
(b) that there was just one single crucial transfer of immunodeficiency virus from the ancestral animal host (now accepted as the common chimpanzee) to a human being, and that this one event started the AIDS pandemic.
I strongly believe that both preconceptions are erroneous. Let me address them in order.
(a) Although the impact of recombination on phylogenetic dating is hugely controversial, Worobey spends just two sentences addressing it in his latest paper. The key passage of these two sentences reads: ‘Despite initial indications that recombination might seriously confound phylogenetic dating estimates, subsequent work has suggested that recombination is not likely to systematically bias HIV-1 dates in one direction or the other.’
To support this claim, he cites another paper from 2004, on which he is a co-author. It is by Philippe Lemey et al., and it is entitled: ‘The Molecular Population Genetics of HIV-1 Group O’ [Genetics; 2004; 167; 1059-1068, available on-line through PubMed]. In this paper, Lemey and colleagues do briefly address the key published paper which proposes that recombination in HIV-1 does not allow effective phylogenetic dating estimates of that virus to be made. This latter paper is by Mikkel Schierup and Roald Forsberg, and is called ‘Recombination and Phylogenetic Analysis of HIV-1’; it was presented in 2001 at the Lincei conference on ‘Origin of HIV’, discussed elsewhere in this essay. The paper was published in 2003, and appears on pages 231-245 of the conference proceedings.
Paul Sharp, who also spoke at the Lincei conference [see below] was so angry about Schierup’s paper that he declined to allow his own paper to be published in the Lincei conference proceedings. This was probably a wise move, for Schierup’s paper fairly blows apart the arguments of the HIV-1 molecular dating school. It concludes with the telling words that if recombination occurs early in the history of a virus like HIV-1, then ‘it is not valid to use a phylogenetic method to obtain the time estimate’ of when HIV first appeared.
In his 2004 paper, Lemey acknowledges (page 1061) that ‘the results probably indicate significant levels of recombination’ in their dataset. Having noted that Schierup and Forsberg’s 2003 paper arrives at different conclusions from their own, he then proceeds, however, to argue that Schierup’s arguments can be ignored. The basis for doing so actually boils down to the following claim: ‘recombination events in a very rapidly growing population will mostly occur on the terminal branches of the ‘star-like’ sample geneaology.’ [Here Lemey is asserting that most of the recombination in HIV-1 occurs in the more recent sequences (‘the terminal branches’) on the phylogenetic tree of HIV-1 viruses. This may appear a reasonable claim, but further examination reveals its shortcomings; see below.] Lemey goes on to state that although recombination on the terminal branches will result in ‘rejection of the molecular clock and an increase in the variance of TMRCA estimates, importantly, it will not systematically bias estimates of the TMRCA in either direction.’ [TMRCA means ‘Time to the Most Recent Common Ancestor’ – ie the time from the present (2008) back to that start date of 1908, or whatever.]
Later, Lemey effectively repeats this. He once again grants the possibility that recombination might ‘bias the TMRCA upward’ [ie cause scientists to over-estimate the time back to the HIV-1 start date] and also that he and his team might be employing ‘a circular argument’. However, he promptly rejects the latter possibility, again by assertion rather than supported argument.
Lemey and colleagues conclude by claiming that their analysis ‘provides some assurance that recombination is not strongly biasing the estimates of TMRCA’, and that ‘the methods we have used here present a framework that goes some way toward a more realistic description of viral evolution’. But these claims are far from convincing. In fact, the authors do not even appear to be convinced themselves!
I find it astonishing that in his latest (2008) paper, and purely on the basis of Lemey’s 2004 paper on which he was a co-author, Worobey now baldly asserts that ‘recombination is not likely to systematically bias HIV-1 dates in one direction or the other’. All that he has done is driven us a few times round the houses, and then asserted that since recom only occurs in recent sequences, it stands to reason that it cannot affect estimates of the age of HIV-1. If this is not a circular argument, I really don’t know what is. In reality, the Lemey paper entirely fails to address the sort of SIV recombination which I believe took place in the chimpanzee tissue cultures that we now know were being made in the Laboratoire Medical de Stanleyville (LMS).
According to the report of one of the vaccine-makers, Stanley Plotkin, different pools of CHAT vaccine were prepared in the 1950s by adding new tissue culture material in sequence. (He writes: ‘No seed system was used. Rather, each pool served as the seed virus for a subsequent pool.’) [S.A. Plotkin, ‘Unthuths and Consequences’; Phil. Trans. Roy. Soc. Lond. B; 2001; 356; 815-823; see page 816.] This means, amazingly, that any viral contaminants in one vaccine pool would have been passed on and added to the next vaccine pool – and to the next one after that. It is not a technique that would be acceptable today. It is highly likely that if the vaccine-makers adopted such an approach during the important task of preparing brand new pools of vaccine, then the same technique (of adding materials sequentially) would have been employed for the far less crucial task of preparing new vaccine batches.
[Definitions. A pool of vaccine is the term for vaccine that has been prepared to a certain level of attenuation; however, different batches of that pool can be made in different labs, at different times, and in different tissue cultures. By contrast, a batch of vaccine is produced in a single production run. Unlike a vaccine pool, a vaccine batch is homogeneous.]
We have evidence from a military paper from 1958 that refers to the making of chimpanzee tissue cultures (in the US) from the cells of the Lindi chimps, and this paper shows that both kidney cells and sera from the chimpanzees were part of the process. In practice, both kidney cells and primitive preparations of sera will contain SIVs, provided the source animal (in this case the chimp) is SIV-infected. Surveys reveal that 13% of wild central African chimps are naturally SIV-infected, even before any co-caging and gang-caging, which is what routinely happened at Lindi. This means that SIV-infected kidney cells and sera would almost certainly have been added sequentially to the tissue cultures as each new batch of polio vaccine was made at the LMS. It only takes two SIVs in a cell, or in a tissue culture, to spark recombination – and in this case we have the picture of new SIVs constantly being added to the ‘pot’, producing a melange of new SIV sequences and recombinant SIV sequences that would have become more and more complex with time. Given such a background, a 12% genetic difference between two different vaccine batches (one of which infected the 1959 Leopoldville male and the other the 1960 Leopoldville female) would be well within the bounds of possibility.
Crucially, the chimpanzee SIVs so produced (or HIV-1 viruses, as they are known once they appear in humans) would not appear on the more recent ‘terminal branches’ of Worobey’s phylogenetic tree, but would appear right in the centre, in the main trunk. In this core position on the phylogenetic tree, such ancient recombination is, quite simply, undetectable from the perspective of today.
And, as Schierup and Forsberg state in the conclusion of their 2003 paper: ‘if recombination has occurred in the viral population originating from the MRCA, it is not valid to use a phylogenetic method to obtain the time estimate, and our results suggest that doing so would give a certain overconfidence to the previous estimate of 1931 +/- 10 years.’ Their phrase ‘would give a certain overconfidence’ is believed to be polite under-statement, or else a slight Scandinavian misunderstanding of English usage. What is really meant, it would seem, is: ‘would definitely indicate overconfidence’!
(b) Another shortcoming of phylogenetic analysis is that it can only embrace the idea of a single index virus sparking an epidemic. But the concept we have with the OPV theory is entirely different. It is of several different SIV-contaminated batches of CHAT vaccine being administered, within a brief period of time, to ‘volunteers’ in some 30 different vaccination trials across central Africa. In other words, it involves several separate (and near-simultaneous) introductions into humans of variants and recombinants of chimp SIV. From an OPV perspective, this is exactly what appears to have happened around 1959-60, right at the start of the HIV-1 epidemic. Yet the molecular clock supporters are unable to compute two different forms of a virus that crossed over from chimps to humans in the same town at almost the same time. Because of their preconceptions, they are forced to invent an imaginary index virus from decades earlier which (they say) gave birth to both the 1959 and 1960 viruses. The 1959 HIV-1 virus from Leopoldville is almost 12% different, Worobey explains, from the 1960 virus from Leopoldville. He concludes that this is such a big genetic difference that this ‘indicates that the HIV-1 M group founder virus began to diversify in the human population……decades before 1960.’ However, this interpretation is unsupported.
The following explanation is largely based on an e-mailed commentary from one of my ‘advisors’. I reproduce it here with only slight alterations, because it summarises the arguments especially simply and clearly.
‘The key fact that Worobey presents is that in 1959 and 1960 there were in existence in Leopoldville two strains of HIV-1 which had notable differences in their genetic structure. Their interpretation is that the two viruses must have evolved apart from a common ancestor over a considerable number of years. An alternative view is that the origins of HIV-1 lie in chimpanzee cultures that contained a variety of SIVs with considerable genetic heterogeneity. Thus, at the moment of formation, HIV-1 would have possessed considerable genetic diversity inherited from these chimp SIV progenitors. There would have been several separate SIV transfers from chimps to humans via the vaccinations, and what we see in the 1959 and 1960 Leopoldville samples is merely some of this genetic variability of chimp SIV.’
(3) A much simpler explanation for the 1959 and 1960 HIV samples.
Using their molecular clock, Worobey’s team use the 1959 and 1960 HIV-1 samples (and compare them with the 1976 sample, and dozens of other samples obtained from nearer the present, and from different countries around the world) in order to predict that HIV-1 has been in existence since 1908.
If they were not so wedded to these two faulty principles, they might examine a much simpler and more logical explanation. This is that the emergence of the two earliest examples of HIV-1 from the same city (Leopoldville/Kinshasa) and within a year of each other suggests that there might have been a causative event in that city in the years immediately preceding 1959 and 1960.
Was there such a candidate event? There was indeed.
Starting in August 1958, a mass vaccination was staged of all the young children (up to the age of five years) in Leopoldville with CHAT, an experimental oral polio vaccine (OPV). CHAT had been developed by a Polish-American scientist, Hilary Koprowski, who was then director of the Wistar Institute, an independent biomedical research institute in Philadelphia. As I have been proposing in print for the last nine years, there is strong evidence indicating that some, at least, of the batches of CHAT that were administered in Leopoldville (and to a total of nearly one million Africans in the Belgian Congo and Ruanda-Urundi during the late 1950s) were grown in cells and sera from the common chimpanzee (Pan troglodytes).
This species of chimpanzee is host to the nearest viral ancestor to HIV-1. Or to put in another way, the common chimpanzee is the natural carrier of a simian immunodeficiency virus (technically referred to as SIVcpz) which, once it transferred to man, became HIV-1. Some 13% or more of wild chimps from central Africa are naturally infected with SIVcpz, and yet it does not cause any visible disease – presumably because SIVcpz has evolved in the chimpanzee over a lengthy period of time. Clearly SIVcpz somehow got transferred to humans, and this happened in the recent evolutionary past. Because SIVcpz and Homo sapiens have not had the time to evolve together and adapt to each other, the virus causes frank disease in humans, which we call AIDS.
Furthermore, I believe that the genetic difference between the 1959 and 1960 isolates of HIV-1 is exactly what one might expect, given the history of the CHAT vaccinations in the Belgian Congo and Ruanda-Urundi. The Leopoldville vaccinations were carefully conducted in a step-by-step fashion, with new suburbs being called for vaccination every week. Since blood samples from vaccinees, and (rather strangely) samples of the vaccine virus itself, were flown back to the US at regular intervals, this was an ideal opportunity to test and compare different vaccine batches under carefully controlled conditions. And we know for certain that different versions of CHAT were administered in different sections of individual vaccination trials in central Africa during this period. [The supporting evidence for this claim will be revealed at a later date.]
Thus the key question clearly becomes: just how did the transfer of SIVcpz to humans occur?
As I recorded in my 1999 book, ‘The River’, well over 400 common chimps and pygmy chimps (Pan paniscus) were sacrificed during the course of secretive research conducted between 1956 and 1960 at Lindi Camp, some 10 miles outside the Belgian Congo city of Stanleyville (now Kisangani), which is itself 1,000 miles east of Leopoldville via the Congo River. Lindi Camp, one of the two largest chimpanzee holding centres the world has ever seen, was established specifically in order to test and ‘perfect’ CHAT vaccine, and for the first twenty months of its existence only polio work was done there. The nearby Laboratoire Medical de Stanleyville was assigned as the headquarters lab for this research.
Many trials of CHAT vaccine were staged in the Belgian Congo and Ruanda-Urundi before the Leopoldville trial, even if most of these appear to have been conducted in somewhat slapdash fashion, with minimal post-vaccination monitoring of vaccinees. By contrast, the mass vaccination of Leopoldville’s young African children was conducted between August 1958 and April 1960 in a careful step-by-step fashion, with vaccination beginning in different city suburbs on different dates. Samples of the blood of the vaccinees taken both before and after immunisation, together with samples of the vaccine that had been administered to them, were at regular intervals flown back on ice to the USA. One of the implications of this, and certain other important details about the vaccination programme, is that the vaccinators may have been testing, and assessing, different batches of the vaccine in different geographical zones of the city.
It should be noted that one of Hilary Koprowski’s assistants, Stanley Plotkin, took effective charge of this research for a while in the late fifties, and that he paid a month-long visit in May 1959 to the Belgian Congo to inspect and supervise the procedures there.
On the basis of this and other information I have obtained over the past 18 years of research, I strongly believe that the reason why the two earliest (but apparently dissimilar) examples of HIV-1 have been located from a single city (Leopoldville) and within a year of each other is actually quite simple. It is that different variants, including recombinant variants, of chimpanzee SIV were present in the tissue cultures that were used to grow batches of CHAT vaccine locally in the Belgian Congo. (‘Tissue culture’ is the formal name for a monolayer, or sheet, of cells that a scientist may grow artificially in laboratory glassware; such cultures are in turn used to grow viruses, including vaccine viruses, in the lab.)
Despite denials by many of those involved with making and administering the vaccine in Africa – such as doctors Koprowski and Plotkin – I have for some years been in possession of compelling evidence that tissue cultures were routinely prepared from chimpanzees at the Laboratoire Medical de Stanleyville for several years in the second half of the 1950s. (During this period, the use of chimpanzees for making tissue cultures was unique to the Lindi chimps. There is no evidence of chimp tissue cultures having been made from other chimpanzees before the 1960s.) This evidence about chimp cultures being made and used in Stanleyville comes from multiple Belgian and Congolese sources, including the technicians and assistants who were directly involved with preparing them. It also comes from Belgian and American scientists who were involved with this work at a supervisory level. Moreover, on the basis of the latest evidence I have, it seems possible that similar chimp tissue cultures may also have been prepared at the sister lab in Leopoldville, the Laboratoire Medical de Leopoldville.
Finally, let me add a significant detail. Some have pointed out that the mass-vaccination campaign in Leopoldville in 1958-60 was conducted among 0 to 5-year-old children, yet the 1959 and 1960 HIV-1 infections were detected among adults. How, they ask, could an HIV infection pass within a year or so from a child to an adult? Surely this disproves the OPV theory?
In reality, the 1959 sample may have come from an African male of any age. Although in one paper the cohort from which the infected serum was obtained is described as consisting of ‘adults’; in another related paper it is revealed that the actual ages of some of these ‘adults’ run as low as three years! On the other hand, the latest (1960) sample does appear to come from an adult female, so it appears that this question is legitimate, and does need to be addressed.
The answer, however, is fairly simple, for there is evidence that African adults who had been vaccinated with CHAT were present in Leopoldville during the late fifties. The evidence is as follows: (1) I have a document from March 1958 showing that a CHAT vaccination of one specific group of Africans of all ages in Leopoldville city was planned for the near future. (2) One of the two men who was effectively in charge of the vaccinations in Leopoldville has recently confirmed in interview that he cannot recall the identities of all the groups that were vaccinated with CHAT in the city, but that African adults ‘could well have been’ vaccinated.
(3) In any case, it is certain that other adults who had been vaccinated with CHAT arrived in Leopoldville from other places during the 1957-9 period. For instance, the entire population of Tshela in Leopoldville province, a total of 10,000 persons of all ages, were vaccinated with CHAT during this period. Tshela is some 300 miles from Leopoldville city, but much of it is covered by a train link, and there is evidence of a constant traffic of persons between the two places. Indeed, a small outbreak of polio in Leopoldville in the mid-fifties was said to have ‘come from Tshela’!
(4) Dr Michael Worobey – some relevant background.
Over the last few weeks, I have been reviewing my notebooks and papers of the last 10 years, in which there feature many pieces of important information about Michael Worobey, and his involvement in origins-of-AIDS research. This is a brief synopsis of that involvement.
July 1999 (Background) During this month I travelled with my mentor in ‘Origins of AIDS’ research, Professor Bill Hamilton, to Kisangani, the former town of Stanleyville. (Hamilton was a highly-regarded evolutionary biologist then based at the Department of Zoology at Oxford University in a non-teaching role, as a Royal Society professor.) When we arrived, it became apparent that Bill felt we were there primarily to gather faeces from pet chimpanzees, whereas I believed I had made it clear that I would be spending some half of my time there trying to unearth the early history of Lindi Camp and the Laboratoire Medical de Stanleyville. Sadly, we had three fairly volcanic arguments, and by the time we flew home we had still not made our peace together. On the penultimate day in Kisangani, we managed to procure six month visas from the provisional government which at that time held sway over the eastern part of the Congo, which visas were good until January 2000. Bill was keen to revisit the Congo for further research work, but it was clear to both of us that we should not go on another safari together. His conversational French was not especially good, and he clearly needed someone to help him in the Congo, so he began to look around for possible alternative colleagues to accompany him.
Autumn 1999. At this stage Michael Worobey was a Rhodes Scholar from Canada who was doing post-doctoral work in the University of Oxford Department of Zoology. He joined Eddie Holmes’ ‘Viral evolution’ group, which focussed on phylogenetic analysis of viral sequences; in 1999 he and Holmes co-authored a paper together entitled ‘Evolutionary aspects of recombination in RNA viruses’. (Holmes was more balanced than some other molecular biologists on the subject of the origins of HIV, but he still basically subscribed to the tenets of the bushmeat school, and to the work of Beatrice Hahn, Paul Sharp and Bette Korber.) When Bill Hamilton began searching for someone to accompany him back to the Congo, Worobey volunteered, and it was eventually decided that Worobey and his Canadian friend, Jeff Joy, who had experience as a backwoodsman, would accompany Hamilton to the Congo in January 2000 to try to collect faecal samples from wild chimpanzees. Worobey approached Beatrice Hahn in order to ask her advice about the latest techniques of prserving RNA and DNA in faecal samples. The story of their 4-week journey to the Congo, of Hamilton’s contracting cerebral malaria and spending two nights in hospital in Entebbe, Uganda on the return leg, has been told previously. On their return to the UK Bill Hamilton spent one night with his sister in London and then, since he still felt unwell, went the following morning to the hospital of University College London (UCL). While awaiting the results of blood tests, he collapsed with a massive internal haemmorhage and fell into a coma. Tragically, he died six weeks later.
Early 2000. While Bill lay in hospital, Michael Worobey returned to Nairobi, Kenya, where their chimp faecal samples had somehow become marooned in the airport, and brought them back to the UK. At the memorial service in Oxford, Worobey’s contribution was singled out for special praise by that other doyen of evolutionary research in Oxford (and star of television documentaries), Richard Dawkins, who claimed that Hamilton had been going out to the Congo in order to ‘test an unpopular theory’. Professor Dawkins made no mention of the fact that Hamilton was an active supporter of the OPV theory, and it was only due to the intervention of Hamilton’s partner of his last eight years, the Italian science writer Maria Luisa Bozzi, that this misconception was corrected. In a paper from 2001, Dr Bozzi quoted from one of Hamilton’s letters to a Royal Society colleague in October 1999, in which he wrote that he ‘rate[d] the chance at about 95% [that] the OPV theory is right’. But it was now clear that the Oxford University establishment wanted their departed eminence grise presented as an old lion who had the courage to test unpopular theories, rather than as an active supporter of the OPV theory.
2000-2002. During the next couple of years I speak with Worobey several times about his beliefs about the origins of the AIDS epidemic. He presents himself as an open-minded scientist who is not persuaded by either the bushmeat theory or the OPV theory. But he repeatedly stresses one thing: that the effects of recombination on the evolutionary history of HIV has been enormous, and they make interpretation of that history extremely difficult. The attempts to date HIV by means of the phylogenetic clock has created ‘a dog’s dinner’, Worobey tells me on several occasions.
September 2000. The first conference about ‘Origins of HIV and the AIDS Epidemic’ is held at the Royal Society, largely in response to my book, The River, and at the prompting, in late 1999, of Bill Hamilton (who has been described by at least one colleague as ‘the star of the Royal Society’). Michael Worobey is not one of the speakers, but he does attend, and it may be here that he first makes significant contacts with various members of Plotkin’s group, and of the bushmeat school.
September 2001. At the conference on ‘Origin of HIV’, organised (again at Bill Hamilton’s prompting) at the oldest scientific institute in the world, the Accademia Nazionale dei Lincei, in Rome, I have a somewhat heated discussion with that leading proponent of the bushmeat theory and of the molecular clock dating of HIV, Professor Paul Sharp, then of the University of Nottingham. He tells me that Michael Worobey has been to visit Bette Korber at the Los Alamos laboratory in New Mexico, and claims that Worobey now ‘agrees with us’ about the dating of HIV. When I return to the UK, I phone Worobey and ask him where he actually stands. Worobey is angry with Sharp for speaking on his behalf, but he does concede that he has been to see Bette Korber and, rather ambivalently, that he is still making up his mind about the import of their conversations. I find the difference between his account and that of Sharp (who claims that Worobey has already made up his mind) rather interesting. Either someone is mistaken, or else someone is not telling the complete truth.
January 2002. During the first month of 2002, Dr Worobey is filmed by the Galafilm/MFP team that is making a documentary about ‘The Origins of AIDS’. During the filming, Worobey apparently tells the film director that he has been approached by a Belgian group who have managed to acquire ancient tissue samples (in the form of pathology slides) from the Congo. Since Dr Gevaerts, a member of the Plotkin group, first attempted to smuggle such slides out of Kisangani in April 2001, and since I later learn that other Belgian doctors succeed in flying these materials back to Belgium shortly after that, there can be little doubt that the Belgian group is a reference to the Plotkin/Desmyter group, and that this group has been actively collaborating with Worobey and supplying him with materials from the LMS basement since January 2002, at latest. (This is later all but confirmed in a conversation that I have with Dr Jan Desmyter.)
[Background note. The ‘Plotkin group’ is the support group set up by Koprowski’s former assistant, Stanley Plotkin, in late 1999, in his attempt to investigate and discredit the OPV theory. It includes Jan Desmyter, the then head of virology at the University of Leuven (which had closely collaborated with the Congo CHAT research in the 1950s); Dr Dirk Teuwen, a young scientist employed by Aventis Pasteur (the pharmaceutical arm of the Pasteur Institute, now known as Sanofi Pasteur), who in late 1999 or early 2000 is put on paid secondment by Dr Plotkin, the then managing director of Aventis Pasteur, and instructed to make contact with as many as possible of those witnesses whom I had previously interviewed, work which he continues to this day; Dr H. Gevaerts (who made the initial attempt to smuggle the LMS basement samples out of Kisangani in April 2001); and Dudu Akaibe, a vice-dean of science at the University of Kisangani (which had taken over the old LMS building as its medical school) and who is now paid money by Aventis Pasteur to help Gevaerts and others obtain the samples, and to provide other related services.]
2003. The following year, 2003, Bill Hamilton’s former partner, Maria Luisa Bozzi and I exchange many e-mails and have many phone conversations. Finally, in autumn, accompanied by the Australian social scientist Brian Martin (who has attempted to play a go-between role in the origins debate), I drive up to Oxford in order to meet Luisa for what turns out to be the final time. She clearly knows a lot about Dr Worobey from the time that he and Bill Hamilton were preparing their safari together, in late 1999, and she tells me an interesting thing. The previous year, 2002, Mike Worobey apparently told her that he was ‘not going to spoil [his] career because of the OPV theory’. If nothing else, this is a fairly frank exposition of Dr Worobey’s ambition, and how he evaluates priorities in science. During an earlier phone conversation, Luisa Bozzi tells me that Worobey has been telling people in Oxford, including Richard Dawkins, that Hamilton changed his mind about the OPV theory during their trip to Congo together. Worobey’s apparent ‘evidence’ for this seems to be flimsy in the extreme, and Luisa apparently expends a lot of energy trying to put the matter straight with Dawkins and others. Clearly Luisa Bozzi is becoming increasingly horrified about the political shenanigans that have become intertwined with the origins debate, and in the end she decides not to appear in the MFP film. I have the copy of a draft of an e-mail she intends to send to the film team, in which she seeks to explain why, instead of appearing on camera, she prefers to answer some of their enquiries in writing. She writes: ‘As Bill Hamilton’s partner of the past six years, I feel it my duty to protect his reputation, his integrity and his immense effort to find the truth…..from any misinterpretation, manipulation [or] false report of his beliefs and behaviour.’ Another of her responses relates to the relationship between Bill Hamilton and myself, and here she writes: ‘Bill Hamilton’s ideas about the OPV theory were based on the research made by Ed Hooper on this subject, due to a very strong intellectual relationship between them.’
August 2003. During the same year, Dr Worobey is rather unexpectedly (for one so young and relatively inexperienced) appointed an assistant professor, and head of his own lab at the Department of Ecology and Evolutionary Genetics at the University of Arizona, in Tucson. He apparently takes with him the research into ancient HIV that he has previously been conducting at the University of Oxford. Before arriving in Tucson, he revisits Kisangani in the Congo, where he organises further research collecting wild faeces from chimpanzees in the Parisi Forest, near Kisangani. It appears probable that during this visit to Kisangani he also organises collections of blood samples (for HIV and other testing) from the human population, as well as further access to the crucial 1950s samples from the
April 2004. Worobey publishes his first major scientific contribution on the origins of HIV debate in the form of a letter to Nature co-written with the two scientists who have championed the bushmeat theory: Paul Sharp and Beatrice Hahn. The letter is entitled ‘Contaminated polio vaccine theory refuted.’ Amusingly, this is the third time that that august scientific journal, Nature, has allegedly refuted the OPV theory, each time on false grounds; it has never, however, published any version of the theory written by a proponent. On this occasion, Worobey’s argument is that an SIV he has obtained from the faeces of wild chimpanzees from the Pan troglodytes schweinfurthii (Pts) subspecies found in the Parisi Forest, 70 miles south-east of Kisangani, is slightly less similar to HIV-1 than are SIVs found in chimpanzees from the Pan troglodytes troglodytes (Ptt) subspecies from Gabon, Congo Brazzaville and Cameroon, 500 miles or more to the west. He goes on to claim that the chimps taken to Lindi Camp in the 1950s were all from the vicinity of Stanleyville/Kisangani, and that his one SIV sequence from a Parisi Forest chimp therefore refutes the OPV theory. The argument is transparently wrong. The ‘Lindi chimps’ were indeed mostly from the Pts subspecies, though they also included bonobos or pygmy chimps (Pan paniscus). However, the Lindi chimps were collected from a wide swathe of rain forest covering more than 200,000 square miles, and extending as far west as Coquilhatville, now Mbandaka, which was a known collecting centre for the very type of Ptt chimps, from Congo Brazzaville and Cameroon, that Worobey and Hahn argue are the only true hosts to the ancestral virus of HIV-1. My carefully-understated 300-word letter to Nature disputing the claim that the OPV theory had been refuted was (as usual with Nature) rejected for publication. (However, two years later, I obtained further documentary evidence showing that at least one Ptt chimpanzee from the Gabon/Cameroon/Congo Brazzaville area was definitely present among the experimental chimps at Stanleyville. Because there was co-caging at Lindi camp, and because there was a play-cage where chimps and bonobos from different sources were put together, this one historical detail blows apart Worobey’s ‘wrong chimpanzee’ argument.)
April 2004. I have two phone conversations with Maria Luisa Bozzi in the wake of the Nature letter. She tells me that ‘if Bill had still been alive, Michael Worobey wouldn’t have published this.’ She is quietly furious about the role that Worobey has played, and for the first time she spells out what she knows. She tells me that Worobey has in reality been an opponent of the OPV theory from at least 1999, when he first made contact with Bill Hamilton. It is thus confirmed that throughout the time Worobey and I were in contact (ie from 2000 to 2002), he had misrepresented himself to me as someone who was still open-minded about how AIDS started, and who believed that the molecular dating of HIV was a ‘dog’s dinner’. Luisa also told me that she was feeling tired, and did ‘not want to be involved in this controversy’ any more. Less than 2 weeks after our second conversation, Luisa Bozzi dies suddenly and tragically at the age of 64, after an unexpectedly severe asthma attack.
2006. I am provided with information which proves that Worobey’s team has been quietly sampling chimpanzee stools from many different places in the Democratic Republic of Congo since at latest 2004, and that many (it would appear some dozens) of these faecal samples have tested positive for SIV. One wonders why, four years or more since the start of that research, Worobey has still published not one word about this copious evidence about SIV-infected chimps from the DRC – especially when collaborators of his are claiming that the only evidence of SIV in Congolese chimpanzees is that one virus from the Parisi Forest, and that further surveys have drawn blanks.
October 2007. Worobey publishes a paper that misleadingly claims (by molecular dating, once again) that HIV-1 travelled from Congo to Haiti, and then from Haiti to the US in about 1969, years earlier than previously thought. I respond with a paper on this site entitled ‘Worobey’s wobbly research’, which points out the shortcomings in this work, and the fact that any one of three theories is still viable about how HIV arrived in the US.
October 2008. Worobey publishes his latest letter in Nature. Once again, the conclusions appear to be driven by his scientific ambition, rather than by a genuine attempt to unravel the truth.
What is significant is that the co-authors on his latest paper include Dirk Teuwen from Stanley Plotkin’s group, which is the first time that Teuwen has been openly identified as a Worobey collaborator. However, the information from 2002 (and since) makes it clear that Teuwen and Worobey have been working together for nearly 7 years.
Worobey’s co-authors also include a man called Jean-Jacques Muyembe, who is a senior pathologist at the University of Kinshasa. According to certain sources, Dr Muyembe was instrumental in recovering the crucial HIV-infected lymph-node sample that was apparently originally provided by the Leopoldville woman in 1960. My information is that Jean-Jacques Muyembe has had close links with US scientists since 1976, when he was the leading Congolese doctor who accompanied the US military teams up to the village of Yambuku during what then appeared to be the world’s first epidemic outbreak of the deadly Ebola virus. (There had in fact been a prior epidemic in Sudan, starting just a few weeks earlier.) In those days African names had been subjected by the US-backed dictator of Zaire (now DRC), Joseph Mobutu, to ‘Zairification’, and Dr Muyembe was known as Tam-Tam Muyembe. But this man is the same Dr Muyembe who, according to the reports I have received, travelled up to Kisangani some years ago and actively assisted in the activities of the Plotkin group. Apparently he helped persuade scientists at the University of Kisangani that they should release some of the remaining tissue samples from the Laboratoire Medical de Stanleyville (LMS) basement to him. These seem to have been passed on to Michael Worobey, who has allegedly now also taken possession of the remainder of those samples. During his Kisangani visit Dr Muyembe also apparently participated in interviews with some of the past witnesses from Lindi camp and the LMS. In some of these interviews, witnesses were apparently pressured or encouraged financially (ie bribed) by some of the doctors present, in order to change key aspects of their stories. It is not known whether or not Dr Muyembe was personally involved with the latter process.
I have since spoken with one of these witnesses again by mobile phone, and was able to identify two or three details on which he now gave a different story from that which he had originally given us on camera and tape recorder in April 2001. Fortunately, however, not all the African witnesses so approached were willing to change their stories after being seen by the Belgian and Congolese doctors who were collaborating with Desmyter, Plotkin and Teuwen. It appears that only two of these witnesses bowed to temptation, and that the key elements of the accounts we gathered from Kisangani in 2001 have survived intact.
(5) The ongoing cover-up.
To sum up, it is now clear that there is a substantial cover-up going on about the CHAT research that took place in Stanleyville/Kisangani in the 1950s – and that that cover-up began back in the 1950s. Certain specific details are now apparent, among them the following…..
A) Michael Worobey, whether wittingly or unwittingly, is now a key member of a Belgian-American cover-up, designed to protect the people who made and administered the suspect oral polio vaccine that appears to have introduced SIVcpz (chimpanzee SIV) to the human population, where it became redesignated as HIV-1. Unfortunately, it is now quite apparent that the cover-up is also designed to protect the governments that authorised and backed the testing of this experimental vaccine in the 1950s in nearly one million African ‘volunteers’. (Like several other of the proponents of the bushmeat hypothesis, Professor Worobey benefits from substantial grants from government and private foundation sources. For instance, the laboratory of the misguided coordinator of the bushmeat school, Beatrice Hahn, currently enjoys a $5 million grant from the Gates Foundation. This raises the question of whether one of the functions of philanthropic donation is to safeguard one’s corporate interests, through avoiding deviation from a clearly-held governmental line on controversial or ‘difficult’ issues.) And it is clear that Worobey has, since 2003, been fast-tracked both by the US government (which in 2003 awarded him an assistant professorship and his own lab in Tucson, Arizona), and by pillars of the scientific establishment such as Nature, which has highlighted Worobey and his work since 2004. The hand of Robin Weiss (who still effectively controls HIV/AIDS coverage in Nature) may be detected in the latter process.
B) Dr Worobey has, since 2001 or early 2002, been acting in collaboration with those Belgian doctors (such as Dr Jan Desmyter, Dr Gevaerts and Dr Dirk Teuwen) who made the initial attempt to smuggle the LMS basement samples out of Kisangani in 2001. The aforesaid Belgian doctors are acting in direct
collaboration with Dr Plotkin; indeed Dr Teuwen’s investigations have been paid for by Dr Plotkin, via Aventis Pasteur (now Sanofi Pasteur). Worobey also cites Dr Jean-Jacques Muyembe, who is apparently the person who salvaged the HIV-infected the 1960 sample. It is now proven that Michael Worobey (and by all accounts his collaborators in the field of molecular genetics: Paul Sharp, Beatrice Hahn and Bette Korber) are in cahoots with the American/Belgian team led by Dr Plotkin and Dr Desmyter. The former group, the geneticists, are doing everything in their power to persuade people that HIV-1 dates from an era before the OPV trials. And the latter group, consisting of those who developed and administered CHAT vaccine in central Africa, are doing everything in their power to suppress information about the polio research conducted in the 1950s at Lindi camp and the Laboratoire Medical de Stanleyville. The geneticists and the vaccine-makers are all part of the same club, and their researches are all fuelled by the same anxieties and interests. It is my belief that under these circumstances, it is no longer possible to have faith in the accuracy or integrity of any verbal or written statement or claim that emanates from any member of this club.
C) Dr Worobey has had access to the ancient samples from the Laboratoire Medical de Stanleyville basement for nearly seven years now, and in recent years he has apparently managed to obtain all of the remaining samples from that basement. This begs two questions. (a) Why on earth would it be so vitally important to him to corner every last sample that is available? (Clearly it is not in the interests of impartial scientific enquiry if only one partisan group has access to a vitally important set of samples, especially a set which might help illustrate the history and evolution of AIDS.) (b) Why on earth have we heard nothing from him about his analysis of these samples? Even if it should be announced at some time in the future that he has found no HIV in the samples (as one suspects will eventually happen), we have no guarantee that this is genuinely the case. It only requires one bad apple in one of the labs where the samples have been held in the last ten years (not necessarily Worobey or a member of his team) for the historical evidence to be irrevocably contaminated.
D) Even if Dr Worobey later lets other groups test these samples, there will always be concerns that vital samples (including some containing HIV) may have been removed or altered. I always suspected that these samples would include hard evidence that HIV existed in Stanleyville from the time immediately after the first polio vaccinations there. Indeed, there is clinical evidence suggestive of this. I have been warning since 2001 of the risk of malfeasance – and of just one group gaining a monopoly over the samples – and yet that is exactly what has happened. I have been unable to stop the process whereby first the Belgians under Desmyter, and later the team led by Dr Worobey, cornered the market; (and yet, given the historical background, these were the very last groups that should have been permitted to exercise such a monopoly).
E) For many years Beatrice Hahn has been promoting the idea that all the diferent groups of HIV-1 viruses were born in the cradle of Cameroon. But there are many unanswered questions about her Cameroonian research. I am unwilling to go into further details now, but I will point out once again that there are serious shortcomings and snags to her thoery that SIVcpz crossed from chimp to human in the south-eastern corner of Cameroon in (or just before) 1908, and then spread quickly to infect someone in Leopoldville, 500 kilometres to the south, while dying out in the original area of infection. Then Hahn needs to have a roaring epidemic in Leo, which allows ten or so different subtypes of HIV-1 to form, which then begin to recombine with each other (in the 1960s?) to create the HIV-1 epidemiology seen today. All in all, her scenario of origin seems extremely far-fetched. One particularly strange aspect was the publicly-made claim by her associate, Paul Sharp, that there must have been thousands of cases of HIV infection and AIDS in the region between southern Cameroon and Leopoldville in the late 50s. [See also point 5(H), below.] There is not one shred of evidence (clinical, epidemiological or virological) to support this claim, which for a number of reasons seems extremely implausible. My forecast is that sociologists and/or anthropologists working in close connection with the Hahns and Worobeys will soon publish some anthropological/sociological research that attempts to offer support to Hahn’s Cameroonian origin idea, and to Worobey’s latest HIV-1 start-date of 1908. (In similar vein, in early 2000 AIDS Research and Human Retroviruses, a journal over which Beatrice Hahn seems to exercise a considerable degree of control, published an analysis by anthropologist Jim Moore, proposing that colonial medical practices in French Equatorial Africa had sparked the outbreaks of AIDS in the early part of the 20th century. Just weeks later, Korber published her article positing a start date of 1931.)
F) In an interview on the BBC, Worobey expressed the interesting idea that AIDS is caused by humans, having been created when Man started living in big cities. And, he said, if it is made by humans, then humans ‘can drive it back into extinction’. I fail to see the underlying logic in this statement.
G) Note Worobey’s frequent references to his ongoing efforts to unearth other early samples. This would appear to be a carrot to attract further funding. In one of his grant applications he has already stated that he can take the history of HIV-1 back to 1955 (ie just before OPV) or even further. My hunch is that we may expect to hear about other amazing ‘discoveries’ from Worobey in months to come, but that it would be advisable to subject any such ‘discoveries’ to very close scrutiny!
H) The commentary accompanying the Worobey article is written by Paul Sharp and Beatrice Hahn, and entitled ‘Prehistory of HIV’ [Nature, 2008, 455; 605-606]. It is, of course, highly partisan towards the bushmeat version of events, even down to their inclusion of a partisan map. [What is noteworthy, just as in Worobey’s article, is their failure to highlight the key point: that the two earliest samples of HIV-1 in the world, separated by 16 years from the third earliest sample, were obtained from the same city within the span of a single year. This, in turn, allows them to avoid even mentioning possible alternative explanations, and in particular the OPV theory! One wonders whether a neutral commentary would not have been more useful to Nature’s readers.] Moreover, I believe that Sharp and Hahn gloss over the lack of epidemiological support for their position. In particular, I note their casual assumption that ‘there were probably only a few thousand HIV-infected individuals by 1960, all in central Africa. Given the diverse array of symptoms characteristic of AIDS, and the often long asymptomatic period following infection, it is easy to imagine how the nascent epidemic went unrecognised.’ This wholly misguided version of events is very revealing. Yes, if one bases one’s calculations on their bushmeat theory, and if one assumes on their behalf an index infection in 1908 and then ties this to a known infection point in the recent past [say the recorded 3% of the 1980 population of Kinshasa (which was then 2.55M) who tested HIV-positive, which would equate to 76,500 HIV-infected persons in Kinshasa in 1980], this would create a doubling time of about 4.5 years, and we should have reached 1,024 HIV-infected persons by 1953, and 4,096 by 1962. However, on the basis of everything I know about AIDS in Africa, I very strongly believe this level of HIV infection in the late fifties/early sixties to be a fantasy. My reasoning is as follows. Because of other circulating pathogens, the time from initial HIV infection to AIDS (without medical intervention) is typically under five years (let’s for convenience say 4.5 years) in Africa, as distinct from the much-quoted ten years in the West. This means that according to Sharp and Hahn’s origins ideas, there should have been about 3,000 HIV-infected persons, or 1,500 AIDS cases in Leopoldville by 1960. [Their theory demands that HIV-1 ‘cooked’ in the crucible of the large metropolis of Leopoldville, having effectively died out in the intervening areas of Afrique Equatoriale Francaise (AEF, which includes present-day Congo Brazzaville, Gabon and Cameroon), where they insist it started with a Cameroonian crossover in or just before 1908.] But I strongly argue that such a large body of AIDS cases (1,500) would have been recognised in those days of careful, even obtrusive colonial medicine in that final year of the Belgian Congo. In reality, there was no such recognition. A far more plausible scenario involves an initial crossover of different SIVcpz variants via CHAT vaccine in the late fifties, with most of the early AIDS cases being ignored in the 10 to 15 years after Independence in 1960 – years which, especially in the DRC, were highly unstable. To sum up, there is no epidemiological evidence of pandemic HIV-1 or AIDS in the old AEF before the 1980s. By contrast, we now have evidence of two HIV-1 infections in 1959 and 1960 in Leopoldville. As for AIDS, first we have ‘Helene’ (the putative first recorded AIDS case, originating from Lisala, who was picked up in 1962 in Leopoldville/Kinshasa, where she presented at hospital in an already advanced state of illness), after which the next persuasive indications of AIDS are all from the DRC, and begin in about 1975. Once again they are recorded by Western doctors working in Kinshasa. Elsewhere in the CHAT-vaccinated zone, AIDS cases are recorded in Stanleyville/Kisangani and in Burundi by 1976. This is exactly the sort of time-scale for recognition of AIDS one would expect, given multiple introduction of SIVcpz variants into humans in the Belgian Congo and Ruanda-Urundi in the late 50s, and a relatively limited level of medical care in the DRC, Rwanda and Burundi in the years between 1960 and 1975. But it does not match well with the bushmeat people’s introduction place of Cameroon, and introduction time of 1908.
I) The stakes are high. And the big questions now are these. (i) Will the bushmeat people suddenly ‘discover’ another ancient HIV-1 sample from Cameroon or Congo Brazzaville (or some similar place close to their mooted south-east Cameroonian source), a sample that allegedly dates from 1950 (or some similar year before the OPV trials)? (ii) And if they do, will it be genuine, or a mislabelled sample from the Stanleyville basement?
Ed Hooper, October 10th, 2008.
Note: See my piece, ‘See No Evil, Hear No Evil, Speak No Evil’ on Hooper’s first piece on Worobey.