Author: Edward Hooper

The AIDSOrigins Webmaster has just drawn my attention to the following article on the Web. Apparently entitled: The AIDS Conspiracy Handbook, it was written by Juliet Lapidos.

It lists several wacky theories about the origins of AIDS. One of the theories that features is the OPV theory, and Ms Lapidos sums up as follows:

“Hooper’s contaminated polio vaccine thesis sounds less wacky than most conspiracy theories and has attracted support from a few notable academics-including late Oxford professor W.D. Hamilton. But it’s definitely wrong. Hooper says Koprowski got his kidney samples from chimps in the Congo. The problem is that the SIV strain endemic to chimps from that region is phylogenetically distinct from HIV. The offending chimps probably came from Cameroon.”

But the claim that the OPV theory is definitely wrong is itself incorrect. The precise source of the chimpanzees that bore the SIV (or SIVs) that crossed into humans to make HIV-1 is still unproven. Ms Lapidos asserts that they “probably came from Cameroon”, but the truth is that we still don’t know. However, there is documentary evidence that at least one Pan troglodytes troglodytes (Ptt) chimpanzee from the west central African region that includes Cameroon was present among Koprowski’s chimps in the Congo. (In reality, there were probably several such Ptt chimps present, but the one single documented chimp proves the point.) Because these chimps were co-caged and group-caged together, an SIV introduced by one single chimpanzee could have infected many others in the camp. For the OPV theory to work, it requires only one such SIV-infected chimp to provide kidney cells or sera that were used in the vaccine.

I was surprised at that very technical phrasing: “phylogenetically distinct from HIV” in the Lapidos article. Where had she picked up such a phrase, I wondered. But my surprise only lasted until I reached the bottom of the article, where Michael Worobey is thanked for his help. It seems that Dr Worobey is actively trying to discredit the OPV theory on the Web. Of course, one of the best ways of doing that is to try to link it to daft conspiracy theories…..and then for good measure to assert that it’s “definitely wrong”.

In an accompanying article, “HIV-1 in 1908?”, I reveal among other things that Dr Worobey (who writes articles that seek to prove that the OPV theory is “definitely wrong”) has been actively collaborating for the last seven years with the doctors who made and administered the suspect vaccine that was used in the Congo in the 1950s. These include Dr Koprowski’s deputy in that era, Dr Stanley Plotkin. We may also safely assume that Dr Koprowski himself, now 91, is a “silent partner” in the enterprise. Now we see Worobey actively trying to diss the OPV theory on the Web. And he claims that he doesn’t have an agenda!

Sorry, Dr Worobey, but you’ve been found out. Again!!

Ed Hooper. October 10th, 2008.

Slate Magazine

March 19, 2008 Wednesday

The AIDS Conspiracy Handbook

Juliet Lapidos

Barack Obama rebuked his former pastor the Rev. Jeremiah Wright on Tuesday for giving sermons in which he blamed the government for creating a racist state and “inventing the HIV virus as a means of genocide against people of color.” Wright isn’t the first to say that AIDS originated in the White House. Others have attributed the epidemic to a laboratory accident, malnutrition, or even God’s divine will. Here’s a field guide to the most prevalent conspiracy theories:

Government Involvement The belief cited by Wright-that the government invented HIV-seems to have originated during the early years of the epidemic. In 1986, crackpot East German biologist Jakob Segal published “AIDS: USA Home-Made Evil.” According to the pamphlet, scientists at a Fort Detrick, Md., military lab manufactured the disease by synthesizing HTLV-1 (a retrovirus that causes T-cell leukemia) with Visna (a sheep virus). The scientists administered their lethal concoction to prison inmates, who then introduced the disease into the general population. In case you’re wondering, Segal has since been accused of being a Soviet disinformation agent.

Similarly, the aptly named Boyd E. Graves (who calls himself a doctor although he has only a law degree) has postulated that scientists in the employ of the U.S. Special Virus Program modified Visna to create HIV during the 1970s. The government, with help from pharmaceutical company Merck, added the virus to an experimental hepatitis B vaccine, which was given to gay men and blacks in New York and San Francisco.

And then there’s Gary Glum, author of Full Disclosure, who fronts the theory that scientists at the Cold Spring Harbor lab in New York engineered HIV, and that the World Health Organization spread the virus under cover of the smallpox eradication program. Glum believes the virus was created to wipe out, or at least control, the black population. (According to a study released in 2005 by the Rand Corp., more than one-quarter of African-Americans believe the disease was engineered in a government lab, and 16 percent think it was created to control the black population.)

Laboratory Accident Edward Hooper, a British journalist, argued in his 1999 book, The River, that Dr. Hilary Koprowski of the Wistar Research Institute unintentionally caused the AIDS epidemic by using chimp kidneys to produce an oral polio vaccine. The chimps, says Hooper, were infected with SIV (the simian precursor to AIDS). Then, via an experimental mass-vaccination program in the Belgian Congo, SIV made the jump from monkey to man.

Hooper’s contaminated polio vaccine thesis sounds less wacky than most conspiracy theories and has attracted support from a few notable academics-including late Oxford professor W.D. Hamilton. But it’s definitely wrong. Hooper says Koprowski got his kidney samples from chimps in the Congo. The problem is that the SIV strain endemic to chimps from that region is phylogenetically distinct from HIV. The offending chimps probably came from Cameroon.

It’s Not a Virus Among the most popular, and pernicious, conspiracy theories is that AIDS isn’t caused by a virus at all. Peter Duesberg, a biology professor at University of California-Berkeley, has argued that drugs and promiscuity are the principal causes of the disease in the United States. He attributes AIDS in Africa to malnutrition.

South African President Thabo Mbeki has voiced support for the so-called Duesberg hypothesis, and his health minister, Mantombazana Tshabalala-Msimang, has recommended treating AIDS with foodstuffs, like garlic, rather than pharmaceuticals.

God’s Punishment The Rev. Jerry Falwell famously argued that AIDS is a plague sent by God to punish homosexuals and American society for tolerating homosexuality. Jerry Thacker, the publisher of Today’s Christian Teen and other Christian magazines, has also called AIDS a “gay plague” and referred to homosexuality as “the death style.” In 2003, the Bush administration nominated Thacker to serve on the Presidential Advisory Council on HIV and AIDS. He withdrew his name under pressure from gay rights groups and Democrats.

Got a question about today’s news? Ask the Explainer.

Explainer thanks Martin Delaney of Project Inform and Michael Worobey of the University of Arizona.

October 9th, 2008.

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.

(1) Background.

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 LMS basement.

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.

Michael Worobey’s first active participation in the origins-of-AIDS debate is believed to have occurred in late 1999, when Professor Bill Hamilton (a highly-respected evolutionary biologist, then rated by many as the “star” of the Royal Society) was seeking someone to accompany him on his second trip to the Democratic Republic of Congo (DRC) to test the SIV of wild chimpanzees.

Some background. Since I first met him in 1993, Bill Hamilton had been my mentor, and he wrote a powerful and highly supportive foreword to “The River”. In July 1999, after the book was completed but before it was published, Bill and I spent just over a week in the DRC, but we had some quite serious disagreements during the trip, which focussed on whether I was there mainly to help him with the collection of samples from local chimpanzees, or was also there to conduct my own historical research into Lindi Camp and the Laboratoire Medical de Stanleyville. We had obtained visas from the rebel government based in Kisangani (formerly Stanleyville) that were good for six further months, and Bill in particular wanted to return there to do more research. Since he and I were, by late 1999, still going through a cooling-off period (and since I was busy dealing with the response to The River, published in September 1999), Bill looked around for a companion in his own Department of Zoology at Oxford University, and came across a young Rhodes Scholar, Michael Worobey, who suggested that they also bring along a Canadian friend of his, Jeff Joy, who had practical skills and experience of living in the wilds.

(Bill and I spoke regularly by phone in the final weeks of 1999, and good relations were restored between us. I had intended to drive up to Oxford to see him the day before his departure for the DRC, but was prevented when my car broke down. However, we did speak once more together when he called briefly by satellite phone from Africa.)

Hamilton, Worobey and Joy set off for Kisangani in early January 2000. The expedition enjoyed success in terms of locating faeces from wild chimpanzees, but worked less well on a practical level. While on safari Worobey got a scratch on his thumb which became infected, so eventually it was decided that he would return to Kisangani a day and a half before Hamilton and Joy, and carry out some of the chimp faecal samples. According to Worobey he was nearly too late, for by the time he got back to the city he had serious blood poisoning and the thumb almost had to be amputated. Hamilton, meanwhile, was declining to take any malaria prophylaxis, and within a few days he got a bout of what appears to have been cerebral malaria (just as he had done during our safari in July 1999). Shortly before they left Kisangani for Kigali, Rwanda, Hamilton became seriously ill, despite which he frequently refused treatments such as rehydration salts. Finally the Canadians managed to get him on board an onward flight to Entebbe, Uganda, where he was confined to a hospital bed for several days.

Eventually he appeared to have recovered, and the three men flew back together to London. However, after one night spent at his sister’s house, Bill again felt unwell, and was taken to University College Hospital in London. While waiting for blood tests, he experienced a massive intestinal haemorrhage, which was probably sparked by a pre-existing condition – and may possibly have been exacerbated by the aspirins he is believed to have taken to cope with the malaria. He fell into a coma from which he never recovered, and he died six weeks later.

While Bill was lying comatose, Mike Worobey flew back to Nairobi to get hold of the samples of chimp faeces which had for some reason become entangled in Kenyan customs. Later, at Bill’s memorial service, Worobey was praised warmly by Richard Dawkins for the role he had played in the expedition. At that service, Dawkins maintained that Bill was a fair-minded neutral who had gone to Africa to test an unpopular and controversial theory (the OPV theory).

This was misleading, in that by 2000 Bill Hamilton and I had been collaborating on OPV/AIDS research for seven years, and Bill was strongly persuaded that the OPV theory was correct. That the Dawkins account did not gain further credence was largely due to the efforts of Bill’s partner of his last six years, the Italian science writer Maria Luisa Bozzi. She read a paper at the Accademia Nazionale dei Lincei conference on “Origin of HIV” in 2001 in which she quoted from one of Bill’s letters to an Oxford colleague, which stated “I rate the chance at about 95%….[that] the OPV theory is right”.

From the start, I recognised Worobey as someone who was committed to his work, but was less sure about what to make of him on a personal level. He was a member of Eddie Holmes’ evolutionary biology group in the Department of Zoology at Oxford University, which broadly supported the bushmeat analysis and molecular dating claims of Bette Korber, Paul Sharp and Beatrice Hahn. Worobey, however, claimed to be a fair-minded neutral who was not convinced by either theory (bushmeat or OPV). On several occasions he told me that the molecular dating of HIV-1 was a “dog’s dinner” because of its failure to take recombination into account. (He seems now to have set aside these reservations, although his reasons for doing so are not apparent.)

On the other hand, Worobey did not appear to be someone who was inclined to rock the boat. Indeed, he seemed to be in awe of certain leading figures in the origins debate, notably Beatrice Hahn and Robin Weiss, and he defended them vigorously against my charges that they had at times acted unscientifically. Broadly, his response to this seemed to be: “So you think you know more about this than they do, do you?”

At one stage in early 2002, I visited Oxford three times to discuss a possible collaboration with Mike Worobey involving the testing of samples from Africa, but I always made it clear that I was not going to put anything in writing in advance about the source of the samples that I might be able to help to provide. Despite this, I was eventually asked to contribute some paragraphs to his grant proposal, which I declined to do. Worobey apparently took umbrage, for he ignored a series of six e-mails I sent him over the next six months, and then when I challenged him to reply within 48 hours if he wished the collaboration to continue, he sent an inappropriately angry and defensive reply.

Soon after this, Worobey was appointed head of his own lab in Arizona, quite a coup for someone so young. And then in 2004, he published his brief communication in Nature (co-written with Beatrice Hahn, Paul Sharp and others) about obtaining an SIV sequence from a single Pan troglodytes schweinfurthii chimpanzee from the Parisi Forest, some 110 kilometres from Kisangani. In summary, they claimed that the chimp faecal samples gathered during the January 2000 safari with Bill Hamilton had not provided any evidence of SIV, but that urine samples gathered at the same time had given intriguing indications of SIV antibodies. Because of this, Worobey had returned to the Congo in 2003, and had obtained a single SIV sequence from a chimp faecal sample from the Parisi Forest. The SIV in question was apparently similar to pandemic HIV-1, but about 10% less similar to it than the SIV commonly found in Pan troglodytes troglodytes, the chimp sub-species originating from Gabon, Cameroon and Congo Brazzaville in west central Africa, a few hundred miles to the west of Kisangani/Stanleyville. The authors then claimed that the Lindi chimps (which by then I and others had identified as having been involved with the preparation of Koprowski’s OPVs) had originated only from “the vicinity of Stanleyville”. Without more ado they asserted that this one sequence of chimp SIV therefore constituted “direct evidence that these chimps were not the source of the human AIDS epidemic” – and went on to claim that they had “refuted” the OPV theory.

Their claim of having refuted OPV/AIDS was complete nonsense, but as usual Nature (where AIDS coverage is allegedly more or less controlled by Robin Weiss) did not publish my brief and pertinent letter of response.

Amusingly, this was the third or fourth time that claims alleging that the OPV theory had been disproved had been published in Nature and Science, all of them false.

There are several reasons why the claims made in Worobey et al’s “brief communication” of 2004 were incorrect, of which I shall itemise just three:

1. The 400 or more chimps that were used in the polio vaccine research at the LMS and Lindi camp were not just gathered from around Stanleyville/Kisangani (as they claimed), but from right across a region spanning some 200,000 square miles of rain forest, which included areas such as Coquilhatville (now Mbandaka), where there is documentary evidence that Pan troglodytes troglodytes chimps were being collected and sold.
2. It is true that most of the chimps the LMS scientists used came from the Pan troglodytes schweinfurthii subspecies of common chimpanzee and Pan paniscus (pygmy chimps or bonobos). However, there is documentary evidence that the LMS scientists also used Pan troglodytes troglodytes chimps in their research.
3. There is also documentary evidence that chimps and bonobos at Lindi were frequently housed two to a cage, and that up to ten apes at a time used to be placed inside a large play-cage. Onward transmission of SIVs is known to occur when different species are caged together, so clearly there was potential for onward transmission of a Pan troglodytes troglodytes strain of SIV to either Pan troglodytes schweinfurthii or Pan paniscus.

Maria Luisa Bozzi was especially indignant and upset about the partisan conclusions that Worobey and his group had drawn in this Nature paper, which she considered a betrayal. She apparently sent Worobey a courteous note, in which she commended him for publishing something which related (albeit indirectly) to the work done on that final research trip with Bill. However, she also spoke with me twice on the phone during the days that followed, and here she was much more forthright. I still have the notes from one of these conversations. Dr Bozzi said she had always known that the young Canadian was ambitious, and that he had quite clearly been a supporter of the bushmeat theory from the very start, from even before the time of his safari with Bill Hamilton. (If she had always known this, it seems likely that Bill Hamilton would also have been aware of Worobey’s leanings in the debate.)

She also told me that Worobey had been telling people in Oxford (including Richard Dawkins) that Bill had “changed his mind” about the OPV theory during the January 2000 trip. The supposed evidence for this was contrived and flimsy in the extreme, and both Luisa and I concluded that Worobey might have been telling certain people what they wanted to hear.

By an unhappy coincidence, Luisa Bozzi died a few days later, after an unusually severe asthma attack. She was aged 64, almost exactly the same age that Bill had been at the time of his death.

The possibility of impropriety.

I am reliably informed from an anonymous source (with information that is largely confirmed by another source) that the one really old sample of HIV-1 that Worobey has managed to locate dates from 1960, and was allegedly provided by a patient from Leopoldville, Belgian Congo. It appears that he intends to make a molecular comparison between this HIV-1 sequence and that of the famous ZR59 sample of HIV-1 (obtained from a Leopoldville male, allegedly in 1959), and then argue that this “proves” that the HIV-1 epidemic must stretch back to before the time of the polio vaccine trials.

If so, then his analysis will once again be highly contentious. We know that virtually every Leopoldville child aged up to 5 years was vaccinated with Koprowski’s OPVs (the Type 1 polio vaccine, CHAT, and sometimes the Type 3 vaccine, Fox) in the months between August 1958 and April 1960. Older people, including adults, were also vaccinated with these strains of OPV in Leopoldville (Leo) during this period; (I have primary evidence of several such vaccinations). Besides this, a significant proportion of the adults vaccinated with Koprowski’s strains elsewhere in the Congo would be expected to have moved to the capital in the years around Independence, since (a) Leo experienced a huge population influx during those years, and (b) people tended anyway to head for Leo, where there were far better medical services, when they fell sick.

I believe it to be highly significant that (if Worobey’s alleged 1960 sample proves to be genuine) the two earliest samples of HIV-1 come from a place that was so extensively vaccinated with CHAT, and date from the years immediately after the start of the vaccinations.

Worobey’s 1960 sample apparently came from an adult, and many people (myself included, in the past) have concluded that the ZR59 sample must have come from an adult male. However, this is not necessarily so, for other sera coming from the same series of blood samples (also described in the original literature as having been provided by “adults”) have in fact turned out to have come from children as young as 3 years! Given the mass-vaccination of Leopoldville’s entire population of 0 to 5-year-olds between 1958 and 1960, this is potentially relevant.

In 2004, Worobey published his first major origins-of-AIDS article (the infamous “Contaminated polio vaccine theory refuted” communication in Nature) from his new lab at Arizona. Now in 2007 come the further inadequately-supported claims (especially those based on phylogenetic dating theory) in his latest article about the arrival of HIV in the Americas, and in his press interviews.

After publishing two major articles featuring exaggerated assertions about the age and origins of HIV-1, Worobey is now revealed to be a committed member of the bushmeat lobby. Furthermore, it is known from several different sources that he is closely linked to the Koprowski/Plotkin/Desmyter/Korber/Sharp/Hahn support group described below.

Worobey’s undeclared research.

What is most worrying, however, is the other work that Professor Worobey has been doing behind the scenes.

I am reliably informed that in the last year or two he has obtained the remainder of the ancient tissue samples (preserved sometimes in the form of paraffin wax blocks and microscopic slides, and sometimes in formalin, with or without another preservative known as buin) from the basement of what was formerly the Laboratoire Medical de Stanleyville (LMS), which served as the headquarters lab for the CHAT vaccinations in Africa in the late 1950s.

On the basis of the OPV theory, if there is one place in the world where one would expect to find samples of early HIV-1, it is Stanleyville.

But we now know that the people investigating this possibility also have a considerable vested interest in the results. In past publications, every one of them has shown significant bias towards the bushmeat theory, a theory that would fall apart if significant clusters of early strains of HIV-1 were found in Stanleyville in the late 1950s.

In April 2001, when I returned to Kisangani, this time accompanied by a film crew, I made a spirited attempt (with the help of the film-makers, who spoke far more fluent French than I) to ensure that at least a portion of the LMS basement samples would get tested at an independent laboratory. However, every submission we made to the then-Rector of the University of Kisangani (who was effectively custodian of the samples) was roundly rebuffed, and it soon became clear that shortly before our arrival the University of Leuven (represented by the then-head of virology, Professor Jan Desmyter), together with an arm of the Pasteur (where former Koprowski aide Stanley Plotkin occupied an executive position at the Aventis Pasteur pharmaceutical house) had both been in touch with the Rector to make formal requests to obtain access to the samples. It was also clear that the University of Kisangani, and in particular certain senior figures at the University, stood to profit significantly if they agreed to these requests.

Both Plotkin and Desmyter clearly had vested interests in these ancient samples: Plotkin because he had helped mastermind the development of CHAT vaccine and the planning of the African vaccination campaigns, and Desmyter because he had taken over the chair of virology at the University of Leuven, the same Belgian university that had collaborated with Koprowski and Plotkin in the African CHAT trials of the 1950s.

An attempt by a Belgian professor who was present in Kisangani at the time of our visit to illegally smuggle some of these samples out in his suitcase was foiled. It later turned out that this professor, who had been born in Kisangani and visited there annually dispensing Belgian government aid, was also directly collaborating with Plotkin and Desmyter.

This Plotkin/Desmyter collaboration began in late 1999 or early 2000. Together with Dirk Teuwen (an Aventis Pasteur employee who was put on secondment on full pay, and given to Plotkin to help him in his efforts to refute the OPV theory) and Abel Prinzie (a Belgian researcher who had worked on CHAT vaccine in the 1950s at the Rega Institute, a semi-independent commercial offshoot of the University of Leuven), they produced a vigorous defence of the CHAT trials, which they presented in the form of a postscript that was added retrospectively (and under conditions of great secrecy) to the published proceedings of the Royal Society meeting on “Origins of HIV and the AIDS Epidemic”. [S. Plotkin et al., “Postscript relating to new allegations made by Edward Hooper at the Royal Society Discussion Meeting on 11 September, 2000”, Phil. Trans. Roy. Soc. (London) B; 2001; 356; 825-829.]

I had a chance meeting in Antwerp in 2004 with Professor Paul Gigase, a Belgian doctor who had done research in the Belgian Congo and whom I had twice interviewed in the past. He told me that he also had played a role in Plotkin and Desmyter’s effort to obtain the LMS basement samples. Gigase said that in 2001 or 2002, at Desmyter’s request, he had flown to Kisangani with another Belgian professor, Francois Stepman (the head of VLIR, the Flemish aid organisation to the Congo) and acted as a sort of go-between. Among other things, he apparently persuaded the Kisangani professors to release at least some of the basement samples to the Desmyter/Plotkin group. The samples were apparently flown to Europe shortly afterwards, and Gigase told me that “a large number of blocks” were examined at the Pasteur, (presumably at the directions of Plotkin). Gigase clearly believed that Plotkin was bank-rolling the entire investigation (including the parts played by Desmyter and Teuwen) through Aventis Pasteur, and he expressed surprise that since the samples had arrived in Europe there had been no announcements about them, but only deafening silence. He indicated that he was beginning to regret the helpful role he had played.

Gigase also apparently interviewed one of my witnesses, an ex-worker from the LMS, on Desmyter’s behalf. However, Gigase apparently had not taken notes, and at different times he gave me differing accounts of what this man had allegedly said to him.

This is fascinating, because later, after “The Origins of AIDS” documentary was released, two Congolese professors from Kinshasa apparently flew to Kisangani to interview some of the other witnesses featured in that film. I have since discovered that during this process at least two of these witnesses were pressured – one of them through a financial inducement – to change their testimony on key issues. It is not known how successful this attempted cover-up may have been; all I can say is that one Stanleyville witness, at least, appears to have changed his testimony on one key issue after receiving a bribe. However, I have filmed evidence that this man spoke very differently when first interviewed.

But back to the LMS basement samples. In the last year or two, the remainder of these valuable ancient samples from the LMS have apparently been obtained by Michael Worobey, who has clearly taken over the work of testing them from Plotkin and Desmyter. Since Worobey is also dealing with ancient samples gathered from Leopoldville and elsewhere, one hopes that he is being scrupulously careful about the provenance and labelling of the samples.

What’s the worst that could happen?

There are now huge stakes involved in the outcome of the origins of AIDS debate. Under these circumstances, can one be absolutely confident that men like Plotkin, Desmyter and Worobey will issue accurate reports about the presence (or lack of presence) of HIV-1 in the ancient samples from the basement of the Stanleyville lab?

Alternatively, can one be absolutely confident that an HIV-infected slide or block originating from Stanleyville in 1958 will not end up being misreported as having come from, say, Leopoldville in 1955, or perhaps another place and time entirely (perhaps Ouesso in Congo Brazzaville in 1937, or some other place and year that ties in nicely with the bushmeat theory)?

The bottom line is that it only requires the participation of one unprincipled researcher (not necessarily one of the aforementioned persons) to effect a crucial change to the results.

In April 2001 the team that made “The Origins of AIDS” documentary and I did our best to make sure that at least some of the priceless LMS basement samples were distributed to different labs, and there independently tested. Because of the pressures and inducements from the Pasteur and the University of Leuven, we failed to persuade the Rector and his senior colleagues at the University of Kisangani to collaborate. I personally have continued these efforts since 2001, but apparently without success.

The fact that the LMS basement samples have, since 2001 at latest, been effectively under the control of scientists who have already shown that they are committed to one specific outcome (an outcome based on bushmeat theory) in the origins-of-AIDS debate means that there has been – at the very least – an opportunity for impropriety.

Because there is prima facie evidence that the origins of AIDS was a subject that was all but ignored by the medico-scientific community for nearly two decades, and that since 1999 a number of incorrect claims have been promulgated in the scientific literature, even the fact that there has been an opportunity for impropriety is of great concern.

What should have happened, of course, is that all the LMS samples should have been placed under the control of a neutral body (some might suggest a lab run by the WHO), and then aliquots from those samples should have been distributed to a variety of different labs to test. Instead, they have fallen under the control of Stanley Plotkin and his allies.

The fact that these samples were not placed under the control of a neutral and independent body means that there will always be the suspicion that the results may be skewed.

For instance, key early HIV-1 results from Stanleyville/Kisangani may have already been suppressed, and indeed, may never be published in the future.

Furthermore, there have clearly been potential opportunities for mislabelling of samples during the transportation and testing process.

This means that there will now be legitimate doubts about the authenticity of any other early HIV testing results that may be announced in the future.

Afterword.

For the record, I have received an anecdotal report from an unexpected source about the results of the HIV testing of some of these archival materials from the LMS basement, and I am currently trying to obtain confirmation of this information.

Ed Hooper. First version completed November 1^st, 2007; this update version completed January 20^th, 2008; minor changes made and posted on March 19^th, 2008.

My sincere thanks to the four scientists from different disciplines and the one “armchair expert” who have read and made helpful comments on the text of this and the accompanying essay, “Michael Worobey’s wobbly research into the early history of HIV”. I have adopted many of their suggestions, but any mistakes that might exist are my responsibility alone.

EH

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

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

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

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

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

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

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

Hypothesis 4.

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

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

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

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

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

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

The inherent bias of Worobey’s paper.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

The strange dearth of early molecular data from the US.

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

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

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

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

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

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

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

The unique prehistory of Subtype B.

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

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

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

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

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

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

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

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

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

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

This sub-hypothesis would beggar the following questions:

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

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

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

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

Worobey’s wobbly dating analysis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Possible explanations for the phylogenetic dating mumbo-jumbo.

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

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

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

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

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

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

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

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

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

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

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

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

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

The question that the molecular daters prefer not to ask.

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

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

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

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

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

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

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

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

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

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

Has there been a cover-up?

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

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

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

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

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

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

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

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

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

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

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

Michael Worobey’s past and future research.

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

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

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

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

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

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

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

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

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

EH 3/11/07