First Letter to Prof. Iliffe

February 21st, 2006

Dear Professor Iliffe,

I recently heard from a Cambridge undergraduate about the impending publication of your new book about the history of AIDS in Africa. I immediately ordered it through Amazon and it arrived a few days ago.

February 21st, 2006

Dear Professor Iliffe,

I recently heard from a Cambridge undergraduate about the impending publication of your new book about the history of AIDS in Africa. I immediately ordered it through Amazon and it arrived a few days ago.

I would like first and foremost to congratulate you. You have clearly done a great deal of scrupulous research, and there is a tremendous amount of relevant information about the African epidemic collated here, meaning that you have made a welcome and important contribution to the available literature. Of particular note are your descriptions of differing patterns of sexual behaviour in various African regions, which lend real significance to your analysis of the early spread of the HIVs through the continent.

However, as someone who has been researching and writing about AIDS in Africa for the last twenty years, I would also like to offer some comments, and in addition to ask you a few questions. At this point I think I should identify myself. My name is Ed Hooper, and I wrote The River, which you are kind enough to refer to as “a fascinating book” on page 7, and which I am pleased to see that you cite in several places in your references.

I have to say that I was disappointed that, having praised The River, you then disposed of the OPV/AIDS hypothesis in a single sentence, concluding that it had been “ruled out”. Despite the vociferous and repeated claims made by the CHAT vaccine-makers and by other eminent scientists at the Royal Society meeting on origins, and in the pages of Nature and Science, the OPV theory has most definitely not been ruled out. Let me firstly take you up on the two apparent “refutations” of OPV/AIDS that you mention in that sentence.

You state that the “theory [has been] contradicted by negative tests on surviving vaccine samples”, but the samples that were tested were the wrong samples, and are essentially irrelevant to the proving or disproving of the OPV hypothesis. They were from American-made stocks released by the Wistar Institute in Philadelphia, and as I made clear at the Royal Society (RS) meeting, different versions of these vaccines (and indeed, of specific vaccine pools) were made in different labs, based on tissue cultures prepared from different primates. Within months of the RS meeting, I returned to Kisangani (formerly Stanleyville), and discovered some revelatory things. As reported at the meeting on origins at the Lincei academy in Rome in 2001 (and more extensively in the documentary film entitled “The Origins of AIDS”, and in “Dephlogistication” and other essays on the web-site), there is now a great deal of evidence indicating that versions of CHAT vaccine were prepared in Stanleyville itself in the late fifties. Furthermore, there is evidence that they were prepared in tissue cultures made from the cells of common chimpanzees, Pan troglodytes, which species is now all but universally accepted as the natural host of the ancestral virus to HIV-1. [For a discussion of the subspecies of the ancestral host, see “The latest scientific evidence strongly supports the OPV theory”, and my latest essay, “New Claims from Paul Sharp – But Has the Source Of HIV-1 Really Been Located?”, on the same site.]

You also cite “the 1959 case in Kinshasa” as a disproof of OPV/AIDS, which prompts a couple of comments. Firstly, since this was an instance of HIV infection in a blood sample (allegedly collected in 1959 in Leopoldville/Kinshasa) it is, I believe, potentially misleading to refer to it as a “case”. (To most people, surely, “a case” implies a case of AIDS, rather than an instance of HIV infection?) However, even if this had been a case of full-blown AIDS in 1959, it would not have disproved the OPV hypothesis, for CHAT vaccination began in the Belgian Congo in February 1957 and in Leopoldville in August 1958, and there are several instances on record of progression from initial infection to frank AIDS within 12 months. In fact, this infected blood sample actually supports the OPV hypothesis rather than disproves it, for the simple reason that this first example of HIV-1 occurred in a community of which the youngest sector (aged 0 to 5) had been immunised with CHAT only a short time before. Furthermore, as outlined (albeit not detailed!) in the “New Claims from Paul Sharp…” essay, this sample may actually have been taken not from an adult, but from a young CHAT vaccinee. I should probably add that in the opinion of several scientists whom I have consulted, this 1959 viral sequence, ZR59, could well represent the sort of primordial (and probably recombined) virus derived from chimp SIVs that would be expected to have been present in Stanleyville-made versions of CHAT vaccine. Please note also that (as reported in the essay) the blood sample containing this first evidence of HIV-1 Group M in humans was actually collected not in 1959, but at some point between 1960 and 1963. The year of provenance of L70 is not crucial to the phylogenetic dating, which is, in the opinion of many scientific observers, an innately flawed process for HIV-1; [again, see essay]. But it does give some idea of the worrying lack of precision about the provenance of that crucial first sample.

By the way, I note that you seem prepared to question the reliability of the 1931 date from the phylogeneticists when you discuss Preston Marx’s infected needles theory further down page 7, but not to afford the same largesse to the OPV hypothesis! However, I also note (far more happily) that you quote Mikkel Schierup’s observation (again on page 7) that phylogenetic dating of HIV based on a molecular clock “may be of very limited value”. [If you’re interested, Schierup’s later – and much more forthright – article on the shortcomings of attempts to date the epidemic was published in the Lincei volume, and is reprinted on the site.]

To sum up, I believe that you have dismissed the OPV theory far too readily, and moreover on insubstantial grounds. I feel it’s a terrible shame that you did not approach the subject of “Origins” from two different angles, one based on the bushmeat theory and the other on OPV theory, and pointed out that there was still heated debate about which version of events had merit. I feel this even more acutely, given that you had clearly read The River and used it quite extensively as a source, especially its early chapters. As it is, your otherwise splendid book merely offers further sustenance to the ill-supported “official” version of the origins of HIV and AIDS. (Your contribution to that process may very well be inadvertent, but as you will see if you read some of the other articles on the web-site, not all such contributions have been. In fact, a tremendous amount of time, effort and money has been devoted to attempts to suppress the OPV theory through means fair or foul!)

I have a few additional comments to offer. The first involves a couple of well-intentioned warnings about certain sources. On page 10, you quote Joe McCormick’s claim of 0.9% HIV-positivity in 1976 in southern Sudanese villagers. I regret to say that it is my impression that, like too many other details in his very readable book, this appears to be inaccurately recorded. For one thing, on page 185 of the paperback version of his book, McCormick claims that this study relates to 1976, and on pages 190 and 194 he claims it relates to 1979. (It can surely not be both years, for otherwise he would undoubtedly have highlighted that detail.) For a second thing, from what I hear, Dr Brun-Vezinet appears at the very least to be “uneasy” about McCormick’s claims; perhaps she suspects that there might have been some lab contamination. For a third, it is quite extraordinary that, if reliable, such a study was never written up as a letter or paper in a medical journal – not least because, if correct, it would offer substantial support to the contention that there was a low and fairly constant prevalence of HIV-1 existing in widely separated areas of rural sub-Saharan Africa in the mid-70s to mid-80s. As it is, the Yambuku serostudy, combined with the 1962 case of AIDS in the woman from Lisala, and the 1976 case of Grethe Rask from Abumonbazi, lends support to a theory of HIV-1 percolating northwards from the River Congo from the 1960s onwards. This is consistent with both the bushmeat and OPV hypotheses, but it fits better with the latter. (As I’m sure you will remember, one of the key early CHAT vaccinations, almost certainly conducted in 1957 or 1958, though it could have been even earlier, was staged in the town of Lisala.)

The second involves the rather less crucial finding of HIV-1 in two of four persons with KS in Kinshasa in 1972 (also on page 10), a finding that would be reasonable on the basis of other known epidemiological facts from the period. I cannot now locate the file in which I’ve stored my copy of the 1993 source article by Remy, but I do have a vague recollection of having some reservations about this report – reservations significant enough, I believe, to have omitted these two alleged AIDS cases from my own list of cases in chapter 54. I will recheck the original source when I next visit a London library.

I agree with you about the striking difference in HIV-prevalence between the countries on the eastern and western sides of sub-Saharan Africa. Sexual mores may play a part, but so, I suspect, may the infectivity (and perhaps pathogenicity?) of different subtypes. Having written that, however, I should add a rider: I was living in Uganda in 1985-7, and know from experience how politicised the issue of the African epidemic was, from the very start, and even in a country that was commendably open about AIDS, at least in that era. I also know that many African countries under-reported their HIV-prevalence and AIDS cases in the 80s for similar reasons. For this reason, I have always been rather cautious about the HIV-prevalence figures issued from Kinshasa from 1985 onwards. I know that Mann, Ryder and Projet SIDA were there for most of the 1980s, but I still suspect that there might have been quite intense political pressures, resulting in a degree of under-reporting…or misreporting.

For instance, I have a copy of a CDC publication from the end of December 1987, which has the Zairean Minister of Health announcing that 12% of Kinshasa’s 3.5 million residents had been found HIV-positive in a new study. The CDC juxtaposes this with 6.3% in “an earlier survey of 2,400 residents” of the city. So was this a case of the Minister trying to squeeze out some extra foreign aid? Perhaps it was. And yet I also have the draft of a protocol for a copper-bottomed serosurvey of Kinshasa, due to be completed by June 1988, with a pilot study due to be undertaken in five quartiers in January/February of that year. In its preamble, this document mentions 3 studies conducted in 1984 [1 study] and 1986 [2 studies], which found 6.4%, 5.7% and 6.7% HIV infection respectively, an undated blood donation survey which found 8%, and it then adds that “prevalence estimates” from other studies undertaken among “particular sub-groups of the population” ranged “from 4% to nearly 10%”. So I wonder if the Zairean health minister with his 12% was just blagging, or quoting results from a new but poorly-planned survey, or whether, possibly, he was quoting accurate figures from the mooted pilot study which had been moved forward by a month or two. (However, I don’t think the full city-wide serosurvey was ever actually undertaken.) Certainly I recall some apparently anomalous results from the limited HIV-prevalence information that emerged from elsewhere in Zaire during the 80s and early 90s: for some reason over 10% in Basunkusu sticks in my mind!

By the way, I do feel that the Burundian sero-study of 1980-1, to which you refer on page 21, is an absolutely crucial clue to the early epidemiology of the virus. You point out that HIV-1-prevalence was even higher in Bujumbura than it was in Kinshasa in the same year (1980), but you do not pick up the astonishingly high prevalence (nearly 12%) in the small port of Rumonge in 1981 (probably the highest prevalence in any general population in the world at that time, if one may define apparently healthy attendees at health centres as “general population”!). During the preceding four years, if I recall correctly, the great majority of Burundi’s goods had been brought in by road via Kampala and Kigali, rather than by rail and lake steamer via Dar, Kigoma and Lake Tanganyika, which was the previous route. Rumonge had therefore become something of a backwater; this is confirmed by visitors during that period. This (a) makes its extraordinary HIV-prevalence in 1981 all the more surprising, and (b) suggests that the virus may well have arrived in Rumonge some years before the supply route changed in 1977. As you may recall, Rumonge and Bujumbura were among the places involved in a separate vaccination campaign conducted along the shores of Lake Tanganyika in April 1958, immediately after the Ruzizi Valley trial. For some reason this separate campaign was not officially reported in the literature, though its totals of vaccinees were included in the Ruzizi trial figures.

You note that one of the most striking aspects of the Burundian epidemic in the mid-1980s and 1990s was its urban focus, but I’m surprised that you fail to note the very different focus in 1980-1, when there were unexpectedly high infection levels in Rumonge and Kihanga, which I believe would be defined as semi-urban and rural, respectively. I believe that without the OPV hypothesis, it is hard to explain why HIV-1 would have initially caused outbreaks in relatively isolated parts of Burundi such as these, whereas five years later it reached such remarkable concentrations in urban areas.

Finally, I do have a few questions for you, which I hope you will be kind enough to answer.

1) On page 15, you write with respect to Cameroon: “Perhaps because it was probably a site of early HIV evolution, the disease there remained scattered, much as it had in the DR Congo until the later 1970s.” Later, on page 17, you write: “In Gabon and Cameroun, where the epidemic had begun later, there was more growth during the 1990s…” I am having some difficulty following your line of thinking here. If Cameroon was a site of early HIV evolution, then why would that lead to scattered cases and a later epidemic? In my Paul Sharp essay, mentioned above, I note that he argues that HIV evolved in south-eastern Cameroon, but that AIDS evolved in Kinshasa. But this would require the index case (or infectees therefrom) to move quickly to Kinshasa, and to start an epidemic there, but not in Cameroon. If HIV began evolving in Cameroon, as you suggest, then we should find some evidence in Cameroon of early HIV-1(M) and AIDS, and a huge range of subtypes and viral variants of HIV-1(M). In reality we get these things in the DRC, but not in Cameroon. At least, that’s how I view it. I’m clearly not following your thought processes here, so could you please explain further?

2) I’m intrigued that you focus on Cameroon as a probable site of early HIV evolution. Might I ask if you had any advance knowledge of the Paul Sharp/Beatrice Hahn announcement?

3) As a matter of interest, could I please know who your scientific advisers were, by which I mean people who gave you advice on the more scientific aspects of your work, and/or who read the manuscript to check for scientific accuracy?

In conclusion, I would like to state this. I really do admire your book (even if thus far I have read only the first half), which makes me all the more sad that it dismisses the OPV hypothesis so swiftly, and on what I believe to be inadequate grounds. I would like to invite you to read further from materials that I have published since The River (such as the essays on the aforementioned web-site), and I hope that after doing so, you might be prepared to reconsider your position with regard to the various origins theories. If you are willing to do this, then I would also hope that when your book is reprinted (as I’m sure it will be), you might consider making some adjustments to chapters 2, 3 and 4, so as to give a fairer crack of the whip to, and description of, the OPV hypothesis.

In any case, I look forward to hearing back from you, hopefully with some responses to my comments and to the specific questions at the end of this letter.

With best wishes,