The Origins of the AIDS Pandemic

A Quick Guide to The Principal Theories and the Alleged Refutations

PREAMBLE: The oral polio vaccine (OPV) theory of origin of AIDS proposes that an experimental OPV made in a unique manner was administered to nearly one million Africans in the 1957-1960 period, leading to the infection of perhaps 10 to 500 people from the former Belgian Congo and Ruanda-Urundi with the pandemic strain of HIV-1, thus initiating the AIDS pandemic. (UNAIDS has proposed that by 2010 over 80 million people had been infected with HIV-1, of whom some 46 million had died from AIDS. Even if some statisticians claim that the true figures are nearer to two thirds of these, AIDS still represents the most disastrous infectious disease epidemic that our species has ever experienced.)

Certain opponents of the OPV theory have sought to personalise it as “Ed Hooper’s theory”, but the theory had already been proposed, discussed and published by many others (such as Louis Pascal, Jennifer Alexander, Mike Lecatsas, Blaine Elswood, Raphael Stricker and Tom Curtis) in the years 1987-1992, before I first heard about it in the summer of 1992. I compared it with the 15 or so other theories of origin I had been examining from 1990-1992, and found that (apart from the default bushmeat theory, which has it that HIV-1 was acquired by a human during the hunting of chimps or the preparation of chimpanzee bushmeat) this was the only hypothesis that stood up to scrutiny. In the years since 1992, I and many others (including the great evolutionary biologist, Bill Hamilton) have examined further evidence from many different sources, and found that OPV is in fact a far more compelling theory of origin than bushmeat. We now know that roughly 15% of at least two subspecies of wild chimpanzees are naturally infected with a simian immunodeficiency virus (SIV) that is closely related to HIV-1. What has been crucial in the years since 2001 has been the gradual gathering of evidence from many different sources that batches of the experimental OPV were prepared locally in Africa in the cells of common chimpanzees and bonobos.

Let me now examine the two origins theories in a little more detail.

The bushmeat theory proposes that at some time near the beginning of the twentieth century a bushmeat hunter, or someone who was handling chimpanzees or chimpanzee bushmeat, became infected with an SIV from a common chimpanzee. Bushmeat theorists believe that this can only have happened in the range of Pan troglodytes troglodytes (Ptt), a subspecies of the common chimp that is naturally found in the present-day countries of Cameroon, Congo Brazzaville, Gabon, Equatorial Guinea and the Central African Republic in west central Africa. They also currently believe that the crucial cross-species transfer happened between 1884 and 1924. They believe that the first human infectee (whom they might call the “index case”) was infected with the ancestral virus of the present-day AIDS pandemic, a virus which they call “HIV-1(M)” (with the M standing for Main group). In itself this is perfectly reasonable, for many other zoonotic diseases start with a single event when a pathogen is passed from an animal to a human and survives long enough in its new host to allow transmission to other humans. Because a cut in the skin would facilitate the passing of blood infections from chimp to human, the bushmeat theory has also previously been called “the cut hunter theory”. Since 2008, proponents of the bushmeat theory have specifically proposed the remote south-eastern corner of Cameroon as the place that represents the hearth of the epidemic, the place where they believe the initial chimp-to-human crossover occurred. However, they believe that after transferring to Homo sapiens, HIV-1(M) moved some 600 miles southwards to Leopoldville (“Leo”, now Kinshasa in the Democratic Republic of Congo), and that once arrived in that large urban centre the virus silently spread, via sex or non-sterile injections, and diversified, a process which they believe must have taken between 30 and 75 years. They believe that HIV-1(M) then burst forth from Leo at around the time of Independence (1960), with the result that at least ten of the very different strains of virus that had developed in Leo became established as the ten major subtypes of HIV-1(M) that are recognised today. They believe that these ten or more HIV-1 subtypes began spreading around the world, with founder effect favouring different subtypes in different places, and that this eventually resulted in the recognition of AIDS as a new disease syndrome among gay men in California in June 1981. (This “Euro-American epidemic” among gay men and intravenous drug users was almost completely caused by HIV-1 subtype B, a variant which it would appear did not survive in Africa itself; the only subtypes B viruses found in Africa today appear to have arrived later on, and to have been re-imported from the West,) The bushmeat proponents believe that to date three other AIDS outbreaks resulting from different variants of HIV-1 (which they call HIV-1 Groups N, O and P) have started at other places in the Ptt range, and that some 10 outbreaks or epidemics of a second and less pathogenic AIDS virus, HIV-2 (Groups A to K), have occurred in West Africa, between Senegal and the Ivory Coast, as a result of the handling of sooty mangabeys or sooty mangabey bushmeat.

By contrast, the oral polio vaccine (OPV) theory proposes that an experimental OPV that had been locally prepared in chimpanzee cells and administered by mouth, or “fed”, to nearly one million Africans in vaccine trials staged in the then Belgian-ruled territories of the Belgian Congo and Ruanda-Urundi between 1957 and 1960, represents the origin of the AIDS pandemic. It provides a historically-supported background: that between 1956 and 1959 over 500 common chimpanzees (Pan troglodytes schweinfurthii and Pan troglodytes troglodytes) and bonobos or pygmy chimpanzees (Pan paniscus) were housed together at Lindi Camp (near Stanleyville in the Belgian Congo, now Kisangani in the Democratic Republic of Congo, or DRC). It proposes that in the Laboratoire Medical de Stanleyville (LMS) the kidney cells and sera of these different chimpanzee species and subspecies were used to prepare batches of CHAT vaccine, but that the fact that the vaccine was locally prepared was concealed by the scientists involved, and has been covered up ever since. (In the 1950s, in most countries around the world the kidney cells of Asian macaques were used for polio vaccine preparation. The use of chimpanzee cells and sera for vaccine preparation was a unique development, but it did not conflict with the 1950s recommendations of the WHO, which were that any suitable primate species could be used to produce polio vaccines.) Of particular importance is the fact that the different species and subspecies of chimpanzee were placed two to a cage at Lindi Camp, to encourage the more nervous pygmy chimps to learn to eat like the common chimps, and that there was a play-cage where up to 10 chimps at a time were placed. Thus there was every opportunity for the onward transmission of viruses like SIVs, through fighting, scratching, the licking of wounds, or coprophagia, the eating of faeces. One of the major vaccination campaigns with the experimental OPV (a version of CHAT vaccine, developed by Hilary Koprowski), was staged in the Belgian Congo capital of Leopoldville in 1958-60, and involved all the city’s children aged up to five years. However, there is evidence that at least some African adults were also vaccinated in the capital, just as some 170,000 African adults were vaccinated elsewhere in the Belgian Congo and Ruanda-Urundi. Nearly forty years passed before it was confirmed by genetic sequencing that the first two cases of HIV-1 infection found in the world had occurred in the Belgian Congo – in fact both isolates came from Leopoldville, in 1959 and 1960. [To give some perspective, these two isolates are sixteen and seventeen years earlier than the next earliest isolate of HIV-1(M), which also came from the DRC, and roughly two decades earlier than any HIV-1 isolate from outside the DRC.] The correlation between the feedings of experimental CHAT vaccine in Africa and the first outbreaks of HIV infection and AIDS in the world (which occurred in the same towns and villages a few years later) is “highly significant” in statistical terms. The OPV theory ascribes the minor outbreaks of AIDS caused by other variants of HIV-1 (Group O, Group N and the more controversial “Group P”) to other polio vaccines (both oral and injected) that were prepared in the cells of chimpanzees and administered in French Equatorial Africa (including Congo Brazzaville and Gabon) in the same late fifties period. It ascribes the outbreaks of AIDS from HIV-2 (of which it maintains that only two were epidemic outbreaks) to other polio vaccines (both oral and injected) that were prepared in the cells of sooty mangabeys (or other monkeys that had been caged with sooty mangabeys) and administered in French West Africa in 1956-60. All the other HIV-2 groups that are claimed by the bushmeat theorists have infected just a single person, and some OPV theory supporters argue that dead-end, non-transmissible infections such as these are the natural fate of SIVs that infect human beings via the bushmeat route: that unless they are introduced in an artificial manner (as via a vaccine), they simply die out.

The above synopsis includes the detail that the use of chimpanzees to make these experimental polio vaccines was kept secret. The OPV theory proposes that the main reason for such secrecy back in the 1950s was that the killing of hundreds of the closest relatives to man (chimpanzees) to produce human vaccines was even then highly controversial, especially when it was being done in a country (the Belgian Congo) where the Belgian royal family had pioneered the conservation and protection of wild animals. Clearly the use of chimpanzee cells involved great potential risks (that humans might acquire a latent virus from their closest primate cousins) and great potential benefits (if the method produced an effective vaccine, then this technique might end up making the vaccine developers a great deal of money). The reason for the ongoing secrecy today is almost certainly the concern in “high places” that if the OPV theory should ever come to be proved, it would fundamentally shake public confidence in the integrity and reliability of the medical establishment, possibly leading to class action law-suits involving billions of dollars. It would also very likely undermine the future use of developing countries as a testing site for experimental vaccines.

There are two subsidiary theories that seek to explain the perceived sudden acceleration in the rate of spread of HIV-1 after it had transferred from chimpanzee to man. These are not theories of origin, but rather theories of early spread. One is the theory of Preston Marx and Ernest Drucker that a sudden increase in the use of unsterilised needles for vaccinations and injections was the crucial factor. The other is a more general theory proposing that it was urbanisation (and in particular the rapid growth in population of a town such as Leopoldville) that played the crucial role. Although technically these secondary theories can be added on to either the bushmeat or the OPV theory, they are in practice normally only added to the former, because without one of these auxiliary theories, bushmeat is hard-pressed to explain why the SIV of the chimp (and indeed the sooty mangabey) suddenly began infecting humans in the twentieth century, when it had never apparently done this in the several hundreds of thousands of years before the twentieth century. In practice, the OPV theory has no need for either of the auxiliary theories, because it proposes that it was the late 1950s vaccination campaigns that explain both the introduction of HIV-1 and the sudden explosion in HIV-1 growth caused by an estimated 10 to 500 initial infectees. In fact, OPV theorists are sceptical about both of the auxiliary theories, feeling that if either one were correct, they would probably have resulted in a recognised epidemic of AIDS many years earlier, for instance in the first half of the twentieth century.

Since the conference on “Origins of HIV and the AIDS epidemic” held at the Royal Society in September 2000, the supporters of the bushmeat theory have repeatedly claimed that they have “disproved” or “refuted” the OPV theory.

There are four major claims made by members of the bushmeat school to support its assertion that the OPV theory has been refuted, which I list below, together with my responses.

Bushmeat claim (1): That samples of the oral polio vaccines used in the Belgian Congo have been tested, and found to be free of HIV, SIV, or chimpanzee DNA.

This claim is untrue. Some of the OPV samples that were tested in 2000, in response to the publication of The River, were from the same pools of vaccine that were used in Africa in the late fifties. But it is batches of vaccine, not pools of vaccine, that are homogeneous (consisting of the same material). The vaccine samples that were tested in 2000 had all been prepared in the US or Europe, and had never been anywhere near Africa. The vaccine batches which are suspected of involvement with the birth of the AIDS pandemic were prepared locally in African laboratories, and although samples of these batches were reportedly returned to the USA for testing, none of these samples has ever been released for independent analysis.

Bushmeat claim (2): That genetic analysis based on a molecular clock proves that the first HIV-1 [the so-called Most Recent Common Ancestor, or MRCA, of the pandemic AIDS virus, HIV-1(M)], existed in the first two decades of the twentieth century, at least 30 years before the OPV trials.

This supposed refutation is merely a hypothesis, and is based on false and circular reasoning. The molecular dating argument depends on the premise that HIV-1 evolved solely by mutation, and that the rate of this mutation can be calculated, thus allowing the beginning of the epidemic to be estimated, or back-dated. Molecular clock dating works well for DNA viruses like smallpox, that evolve almost exclusively by mutation. But a major element in the evolutionary history of SIV and HIV is played by recombination, which is an entirely different evolutionary process, involving the insertion of slabs of genetic material from one viral genome into another viral genome, to produce a completely new virus. HIV is one of most recombinogenic viruses known. In AIDS patients infected with more than one HIV-1 variant at least 90% of the evolution of the virus in vivo occurs through recombination. The same process of recombination would come into play with chimpanzees that were infected with more than one SIV, after the co-caging and group-caging at Lindi Camp. Moreover, there were even better opportunities for recombination in the Belgian Congo, for SIVs contained in the chimp kidney cells and chimpanzee sera used to make tissue cultures for the vaccine at the LMS would be expected to undergo rampant recombination in vitro.

[In vivo: in the living creature. In vitro: in glassware, such as laboratory flask, dish or test-tube.]

The geneticists admit that their molecular clocks cannot model (or make allowances for) recombination, but they claim that they overcome this shortcoming by removing all recombinant HIV sequences from theirdatabases before they start their calculations. However, recombination that occurs early in the life history of a virus cannot be identified as recombination, so this claim is untrue. Nowadays the phylogeneticists working with HIV resort to devices such as “relaxed molecular clocks” in an attempt to bolster their arguments, but it is all hypothesis, not the hard evidence that they frequently claim it to be. The only hard evidence with regard to the origins of the human virus is this: that the two earliest samples of HIV-1 have both been obtained from the same city, Leopoldville in the Belgian Congo (nowadays Kinshasa in the DRC), in 1959 and 1960. 1959 is two years after the experimental OPV vaccination trials began in the Belgian Congo, and one year after they began in Leopoldville.

Nota Bene. I have recently been involved in a protracted email correspondence with a long-time researcher at one of the five or six labs which regularly report on the phylogenetic analysis of HIV in the scientific literature. This man is considerably more open than many of his colleagues, and having a candid discussion with him has been useful; he has had the opportunity to challenge me, and I have had the opportunity to highlight several of the inherent flaws in the phylogenetic analysis of HIV-1, and in the bushmeat theory. After several exchanges, he informed me that the phylogenetic dating evidence would only be consistent with the OPV theory if “10 to 100 transfers” of chimpanzee SIV to humans had occurred in about 1960. But this, of course, is exactly what the OPV theory proposes. The Stanleyville OPVs were grown in locally-prepared chimpanzee tissue cultures that afforded a near-perfect medium for recombination, thus allowing different chimp SIV strains to produce new and different viral variants. The administration of these OPVs in 30 or more vaccination trials in central Africa in 1957-60 (some of which, such as the 6-week Ruzizi Valley trial and the 21-month Leopoldville campaign, took place over lengthy periods, and must therefore have involved making many different batches of vaccine) might indeed be expected to result in the near-simultaneous introduction of perhaps 10 to 100 different variants of SIV to humans in 1957-60. (The figure of “100” is probably an over-extrapolation, but is meant to allow for the ten recognised Group M subtypes and for any other unique strains – meaning strains that appeared not to be part of an existing HIV-1 subtype – that might have existed in the Congo by 1960.)

This is exactly what one geneticist who was consistently open to the OPV theory, the late Gerry Myers, proposed at the Royal Society conference; [Phil. Trans. R. Soc. Lond. B; 2001; 356; 877-887; see web-site]. He pointed to evidence suggesting that a “punctuated” or “synchronised” event (such as a vaccination campaign) had taken place in around 1960, leading to what he called the “sun-burst” of different HIV-1(M) subtypes in the 1960s. [Professor Myers formerly headed the Theoretical Division (Group T-10) at the Los Alamos National Laboratory, and for its first ten years, from 1987 on, he headed the team of editors that produced what is now called the HIV Sequence Compendium (which contains a database of the genetic sequences of all reported HIVs, plus a series of analytical articles). However, in 1997 chronic ill-health forced him to withdraw from the team of editors. At that point, the HIV Sequence Compendium was taken over by his former deputy, Bette Korber, who promptly enlisted two other well-known bushmeat supporters, Beatrice Hahn and Steve Wolinsky, to join the eight-strong editorial team. I have recently learnt that Gerry Myers died in 2010, and I would like to thank him for his principled and courageous contribution to the origins debate.]

Bushmeat claim (3): That the OPV theory is based around “the wrong chimp subspecies”. The bushmeat theory asserts that the AIDS pandemic began in south-eastern Cameroon when a person was infected with the SIV of a Pan troglodytes troglodytes (Ptt) chimpanzee. Bushmeat supporters propose that there were no Ptt chimps at Lindi camp in the Belgian Congo, where the chimpanzees involved with the OPV campaigns were housed, and that therefore the vaccine trials in the Belgian Congo and Ruanda-Urundi could not have been the cause of pandemic AIDS.

These claims are also untrue, mainly because Ptt chimps were present at Lindi Camp, probably in considerable numbers. The evidence produced to date does indeed suggest that the SIVs of Pan troglodytes troglodytes chimpanzees (Ptt, from Congo Brazzaville, Cameroon, Gabon, Equatorial Guinea and the Central African Republic) are the closest known relatives to HIV-1(M), and that the SIVs found in Pan troglodytes schweinfurthii (Pts chimps from the DRC, Uganda, Rwanda, Burundi and Tanzania) are slightly less closely related to the pandemic AIDS virus. However, it is important to note that the SIVs of both chimp subspecies (but almost no other African primates) contain the vpu gene, which is a signature of HIV-1, meaning that the SIVs of Ptt and Pts chimpanzees are the only two close relatives to pandemic HIV-1 found in nature. (It is in fact controversial whether Ptt and Pts should be defined as separate subspecies, for the mitochondrial DNA phylogenetic tree for the two chimpanzees shows Ptt and Pts intertwining on the same branch.)

However, we have documentary confirmation that at least one Pan troglodytes troglodytes (Ptt) chimp was housed at Lindi, for papers published in the 1960s and referenced elsewhere on this web-site describe a Ptt chimp that arrived at Lindi Camp at some point between April 1957 and October 1959. Because of routine co-caging and group-caging policies, the SIV of just one Ptt could have been passed onwards to an unknown number of other chimps, the vast majority of which were sacrificed and any of which could have been used to prepare batches of OPV. And the evidence actually goes much further than that. There have long been several clues indicating that other Ptt chimps were present at Lindi, and the latest findings strongly indicate that in reality, several dozens of Ptt were present there. I am still finding out more about this, and the full evidence will be presented when the time is right.

The same HIV geneticist referred to above recently admitted to me that the claims that the AIDS pandemic started in south-eastern Cameroon are over-confident, and that they make him “angry”. He stated that although the SIV from the south-eastern Cameroonian chimps was the closest match to date to the pandemic AIDS virus, it was still “really quite distant” from HIV-1(M). This man was kind enough to provide Simplot charts that compared different genetic regions of the Cameroonian chimp virus and HIV-1(M), and although he was unwilling to make an estimate, my own estimate for the degree of similarity between the two viruses across the entire genome is approximately 85%. (This compares to roughly 80% for other Ptt chimps and roughly 70% similarity for Pts chimps.) He states that the chimp troupe that gave birth to pandemic HIV-1 might now be extinct. The “south-eastern Cameroonian hearth” story is thus revealed as a convenient fiction, which is very much like the fiction of the 1908 chimp-to-human transfer date. These are inventions based on scraps of evidence and a lot of extrapolation, and they are the sole basis for the semi-coherent but invalid bushmeat theory. It is only by endlessly repeating this fundamentally flawed theory and falsely asserting that it constitutes hard evidence, that the bushmeat theorists are able to claim that the OPV theory must be wrong.

In reality, it may be that a chimpanzee SIV that is really close to HIV-1(M) will never be discovered, and indeed, “the non-human primate ancestor of the AIDS virus” may turn out to be a red herring. If that is the case, then in all likelihood this will be because the way that the pandemic HIV-1(M) virus came into being did not involve blood passing from one chimpanzee to one human in southern Cameroon, but instead involved a series of vaccinations in the former Belgian Congo and Ruanda-Urundi using OPV batches that had been prepared in tissue cultures containing different variations of recombined chimpanzee SIVs.

Bushmeat claim (4): That the chances of a putative SIV in chimpanzee tissues surviving through to the final version of a polio vaccine are trillions-to-one against.

This claim is false, and was based on applying 1990s lab techniques to a 1950s polio vaccine prepared locally in an African lab. The claim was recognised as being fairly absurd even by some of the bushmeat supporters at the time it was made (by John Beale and Florian Horaud, in a paper presented at the 2000 Royal Society meeting. The late Professor Horaud was an old friend of Stanley Plotkin, the former deputy to Hilary Koprowski, the man who developed the experimental OPV, CHAT, and master-minded its testing in the Belgian Congo. Professor Plotkin is younger than Professor Koprowski, and in recent years has taken on the task of coordinating opposition to the OPV hypothesis. Plotkin has hired Dirk Teuwen, an employee of the pharmaceutical house, Aventis Pasteur, of which he was formerly managing director, as his agent in these matters. Some of the tactics used by Dr Teuwen are highly questionable; further details about his role will emerge in due course.

Would a viral contaminant such as SIV survive the vaccine-making process? It should be noted that a different simian virus, SV-40, which contaminated many early versions of both oral and injected polio vaccines has in recent years been detected in the blood of many former vaccinees. Fortunately, being infected with SV-40 is not nearly as serious as being infected with HIV, but SV-40 has been found to be associated with a higher susceptibility to certain specific cancers such as mesothelioma.

To cast more light on the question of whether SIVs would survive through to the final vaccine, let me quote an American virologist who has worked on HIV/AIDS for almost 30 years, from an email written to me in 2003: “An exploded kidney contains macrophages. HIV and SIV reside in macrophages, can be produced by macrophages, and can replicate in macrophages…The plausibility of whether OPV could have been the source [of AIDS] boils down to whether chimps were used on site [ie in Africa] for the production of [batches] used in the human testing.” This man (a no-nonsense virologist with integrity and a straight tongue) thus reveals the paucity of the bushmeat arguments for what they are. If chimps were used to prepare the African vaccine, then without doubt this could explain the current AIDS pandemic. In fact, further comments made by this scientist go much further, and indicate that the linkage is in fact highly likely. There is now overwhelming evidence that chimpanzee cells were used to prepare the vaccine locally in Stanleyville. Some is already in the public domain (for instance in the film documentary, “The Origins of AIDS”), but there is a lot more evidence to come.

Conclusion: It is perhaps useful that two recent books (The Origins of AIDS and Tinderbox) have attempted to put some flesh on the bare bones of the bushmeat theory. As indicated in my reviews of these books, the more that bushmeat supporters try to explain their theory, the more obvious their factual and logical errors become. It should be noted that even now the bushmeat theory is still so vague that it is probably incapable of disproof. However, it is striking that individual planks of the theory are routinely and repeatedly misrepresented or over-stated by its proponents. Good scientists don’t need to make things up, and they admit it when mistakes are found. Many of the bushmeat scientists admit to neither.

However, what the bushmeat supporters are consistently good at doing is publishing alleged refutations of the OPV theory. It is striking that, to date, every one of these alleged refutations have later been revealed as spurious, being based either on errors, misrepresentations, or just plain falsehoods.

Taken as a whole, this gives some sense of the absolute determination by certain powerful people in medicine and other arms of government to see the OPV theory disproved at all costs. The two latest books on AIDS origins have both been promoted and assisted by supporters of the bushmeat theory, and it appears possible that both are part and parcel of a very substantial cover-up.

The “OPV theory is dead” falsehood has also been aided and abetted for more than two decades by the two major scientific journals, Nature and Science, both of which have, since 2000, published only material which promotes the bushmeat theory. Submissions by persons seen to be supporting any aspect of
the OPV theory have all been rejected. It is known that close links exist between on the one hand, some of the vaccine-makers and geneticist supporters of the bushmeat theory and, on the other, Professor Robin Weiss, the scientist who largely controls AIDS coverage in Nature, and who also enjoys a high degree of influence with the editorial board at Science.

The involvement of Weiss is interesting, for he was one of the referees who recommended the rejection of a significant submission about the OPV theory (to Science, in this instance) made by the brilliant evolutionary biologist Bill Hamilton in 1994. In his rejection statement (given anonymously, but certain details in the statement make its authorship certain), Professor Weiss (a) acknowledged that primate kidney tissue cultures are full of macrophages, the very cell type that HIV targets in the body, and (b) pointed out that SIV “contamination” of chimpanzee tissues, if it had happened, would most likely have occurred in central Africa. Reading between the lines, he was proposing that local preparation (in Africa) of a polio vaccine in chimpanzee tissues was at least a viable possibility, and indeed he clarified this idea, writing of “possible use of small batches of experimental OPV made locally”, in his review of The River in Science, dated November 12, 1999. Yet it is this same man (who often seems to act more like a politician than a scientist) who in April 2001 described the OPV theory as “an ugly theory” that had been disproved, and who, as a closing speaker, spearheaded the move to reject the OPV theory at the two origins conferences in London and Rome. When asked to justify his “ugly theory” statement (in a confrontation with myself at the end of the Lincei conference in Rome in September 2001), Professor Weiss was flustered, defensive – and unable to provide any answer.

Despite his claims to the contrary, Weiss comes across as a man who likes to be able to say that he thought of things first. I would freely admit that he took seriously the concept of local vaccine preparation in chimp cells some years before I did. In The River, I considered the possibility that this might have happened (pages 789-791), but finally set it aside in the face of the repeated denials by the vaccine-makers that had made any vaccine locally in Stanleyville. By the time that I started finding hard evidence that local preparation had occurred (January 2001), Weiss was apparently convinced it had not happened, seemingly on the basis of Paul Osterrieth’s “dignified” (as Weiss put it) speech at the Royal Society. In fact, Dr Osterrieth’s brief paper at that meeting was riddled with false claims, errors and contradictions; essentially he claimed that he had made tissue culture, but only in baboon kidneys, and only in mid-1958, about 5 months after I claimed that he had access to chimp tissue culture. The lab was just not modern enough, he claimed, which for a newly-constructed, well-appointed, air-conditioned lab was a bit rich. If Weiss had done even a small amount of checking, he would have recognised that these claims were false. But by that stage, his only interest appeared to lie in trying to close down an “ugly theory”, and in avoiding unwanted embarrassment for some fairly eminent scientific colleagues. It is my belief that Robin Weiss abandoned his primary duty as an honest and thorough scientific arbiter in order to organise the crucial first stage of a politically-acceptable cover-up.

Ed Hooper. April 25th, 2012