Several people have recently asked (either via the AIDS Origins site or via on-line message boards) for my opinions on the latest article about dating the beginning of the AIDS epidemic to Leopoldville/KInshasa in 1920.
The article is called “The early spread and epidemic ignition of HIV-1 in human populations“, and though released earlier on-line, it was formally published in the October 5th, 2014 issue of Science; [2014; 346; 56-61]. Most of the article is consistent with the rest of the work by its authors: the mooted early history of HIV-1 is nothing more or less than computer-generated guesswork.
But the authors have had a major rethink about one of the previous problem areas in their work, and one crucial aspect of their analysis, though they do not advertise it, now aligns precisely with what I have been proposing for several years. In fact, it serves as another powerful confirmation of the OPV hypothesis. All this is explained in more detail in the notes below.
Lead author of the Science paper is Nuno R Faria, who is credited as coming from two of the main centres that support the “bushmeat hypothesis” or “cut hunter hypothesis ” of AIDS origin: the Department of Zoology at the University of Oxford, and the Catholic University of Leuven (KUL) in Belgium. [By contrast, I favour the OPV hypothesis, which proposes that the AIDS pandemic began as a result of the early trials – on approximately one million Africans – of an experimental oral polio vaccine (OPV) which, uniquely, was prepared in the cells of common chimpanzees.]
Many readers of my book “The River” (Penguin/Allen Lane; 1999; 2000) will recognise the Department of Zoology at Oxford as the academic home of Professor William Hamilton, who wrote the powerful Foreword to “The River”, and who from 1993 up to his untimely death in 2000 was my mentor and main scientific supporter. Several members or former members of the Department of Zoology, including Andrew Rambaut, Oliver Pybus and Michael Worobey have been promoting the bushmeat hypothesis since around the time of Hamilton’s death, and one of them, Eddie Holmes, from some years before that. Two of them (Rambaut and Pybus) are co-authors of the present article, and their style and prejudices are clearly visible in its content.
The two senior authors of the piece (who, apart from Faria, are credited with doing most of the work) are Pybus and Philippe Lemey, an investigator in “Evolutionary and Computational Virology” from KUL. Other co-authors are people such as Jacques Pepin and Joao Sousa, both of whom have written extensively on what they describe as the early history of HIV-1, providing historical events that appear to support the timings of HIV-1 and AIDS proposed by the bushmeat school.
The bushmeat, or cut hunter hypothesis of origin proposes that the “AIDS virus”, HIV-1 Group M, emerged from south-eastern Cameroon early in the 20th century (1908 or 1931, according to their two major estimates), and then travelled over 500 miles south to Leopoldville (now Kinshasa) where, the bushmeat scientists propose, it began spreading to others as AIDS became an epidemic and eventually a pandemic. By contrast, the OPV hypothesis points to the trials of an experimental OPV on a million Africans from the former Belgian territories of the Belgian Congo and Ruanda-Urundi: an OPV which, uniquely, was prepared in the cells of chimpanzees. These polio vaccine trials took place in 1957-1960, in the final days of colonialism in this part of Africa, in venues which bear a highly significant correlation with the first appearances of HIV and AIDS in the world.
The bushmeat scientists have repeatedly and falsely claimed that their work has refuted the OPV hypothesis, and this process has been championed by two of the major pillars of scientific publishing, Nature and Science. Since year 2000, these two journals have avidly published numerous articles and promoted numerous news items from the bushmeat school, while refusing to print any article or letter from any supporter of the OPV hypothesis, including myself. I know this, because I have submitted several, and I’ve heard from others of similar experiences.
By publishing articles and news items based on such tenuous data, Nature and Science have promoted a theory that is politically convenient to many senior physicians and scientists, and to certain governments. And by refusing to publish counter-evidence, these journals have betrayed the most basic principles of Science.
Since the publication of the revised paperback version of The River in 2000, I have continued my research and, as I have long been intimating on this web-site, I can now demonstrate (a) that the experimental OPV made in Stanleyville, Belgian Congo in the late 1950s was indeed prepared in the cells of common chimpanzees of the Pan troglodytes species, and (b) that the chimps involved in these experimental procedures included many chimpanzees from the Pan troglodytes troglodytes subspecies, including those that come from the very area of west central Africa which members of the bushmeat group insist is the source of pandemic AIDS.
The former finding is hugely important, proving that the central tenet of the hypothesis proposed in The River was correct. The vaccine-makers continue to insist that they never used chimpanzee cells for the vaccine, but I and others have proved otherwise. (Some of the evidence for this was broadcast in the prize-winning 2003 documentary, “The Origins of AIDS”, but there is considerably more evidence that has not been published to date.) This confirms that the word of the vaccine-makers cannot be relied upon for any of the history relating to these trials. The latter finding, that the chimps used in the African OPV trials included a large number of the Pan troglodytes troglodytes (Ptt) subspecies, has involved many years of investigation and research. I have been surprised by the scale of the evidence that has emerged, which I was not initially either looking for or anticipating. (To begin with I knew only that one of the chimps at Lindi Camp, near Stanleyville, the headquarters of the OPV trials in the Congo, had probably been a Ptt. About 5 years ago I came across the first documentary proof of this. What we now have is evidence that many Ptt were present.)
These are the reasons why I believe that the Faria paper is based on flawed science:
1) The authors of this article, like other bushmeat authors before them, seem to be determined to construct a prehistory of pandemic HIV-1 that precedes the OPV trials in Africa in the latter half of the 1950s. And yet, in an extraordinary twist, they seem to have produced evidence that favours the OPV hypothesis far more than the bushmeat hypothesis of origin.
2) They hypothesise that HIV-1 began in Leopoldville, Belgian Congo in the year 1920. (They actually call Leopoldville “Kinshasa”, though it only gained that name in 1964, four years after Independence. Throughout the article they have used only contemporary place-names, which is not helpful when most of the analysis concerns the colonial era.) Although they make mention of the alleged crossover from chimp to human in south-eastern Cameroon mooted by bushmeat advocates like Beatrice Hahn, there is no mention of Michael Worobey’s mooted crossover date of 1908. Neither is there any explanation of why they have abandoned a 1908 start-date for the epidemic in Cameroon for a 1920 start-date in Leopoldville/Kinshasa.
I strongly dispute the claim by the authors that they have “shown” that HIV-1 was present and spreading in 1920s Leopoldville, meaning that their computer runs have proved it. They have proved no such thing. Their analysis is built around a very imprecise model, a “molecular clock” which is based on the principle that HIV-1 mutates at a constant rate. (It doesn’t. Because HIV-1, a lentivirus and retrovirus, is inherently and massively prone to recombination, it mainly evolves through recombination rather than mutation.) Therefore the bushmeat scientists base their work on a misleading model which produces false results. However the authors, who do not recognise this, have also introduced the questionable concept of a “relaxed molecular clock”, which by providing the results needed to underpin their assertions, somehow seems to behave exactly as they want it to behave. Some at least of my and others’ criticisms of their approach have perhaps been taken on board, for the authors of this latest paper do acknowledge early on that “several aspects of the evolutionary models used remain vulnerable to criticism”. Later, they devote the penultimate section of their paper to an analysis of whether “ignoring recombination” and the use of relaxed molecular clocks can be justified. However, they throw various ideas around for two lengthy paragraphs, and eventually conclude (without very much supporting evidence) that what they’re doing is just fine, and that their assumptions are not affecting their results. But the exercise is inherently flawed. It’s a bit like giving Genghis Khan a couple of paragraphs to explain whether or not he feels that he’s a bad person.
3) Their molecular dating analysis is also flawed in another major way. It assumes that humans initially acquired HIV-1 through a single chimp-to-human crossover of a Simian Immunodeficiency Virus (SIV) that is found in common chimpanzees, and which is acknowledged as the closest ancestor to pandemic HIV-1. The bushmeat scientists assume that this crossover led to the infection of one human index case, which they like to refer to as “The Most Recent Common Ancestor”, or TMRCA. But the concept of TMRCA for HIV-1 is in itself highly controversial. Superficially it sounds believable, but it ignores an equally appropriate hypothesis, that of “punctuated origin”, which was first proposed by Gerry Myers at the Royal Society conference on “Origins of HIV and the AIDS epidemic”, back in 2000. The hypothesis of punctuated origin proposes that a unique event such as the introduction of a faulty vaccine administered in trials in several different places could have led to the near simultaneous infection of many different humans with variations of the HIV-1 precursor. Over 30 OPV trials were staged in Belgium’s African territories between 1957 and 1960, just before the Belgian Congo gained Independence and became the Democratic Republic of Congo. [For Myers’ original paper, see: “The origin of acquired immune deficiency syndrome: Darwinian or Lamarckian?”, by Burr T, Hyman JM and Myers G; Phil. Trans. R. Soc. Lond. B; 2001; 356; 877-887.]
4) The Faria paper baldly reports that HIV-1 then travelled via trains and rivers (but mainly trains) to several Congolese cities: Lubumbashi (then called Elisabethville) by 1937; Mbuji Mayi (then called Bakwanga) by 1939; Bwamanda (in Equateur province, north of Mbandaka) in 1946 and Kisangani (then called Stanleyville) by 1953. It also reports that HIV-1 crossed the river from Leopoldville to what is now often called “Congo-Brazzaville”, to reach the city of Brazzaville in 1937 and the port of Pointe Noire a few years later. (So it seems that the bushmeat scientists are proposing that the initial HIV-1 virus originated in 1908 in Cameroon, and then travelled down from Cameroon through Congo-Brazzaville to Leopoldville in the Belgian Congo in around 1920 and then, 17 years later, crossed back over to Congo-Brazzaville again. Such are the convolutions required by the bushmeat hypothesis!)
5) However, there are major errors in their historical analysis. [Since I am quoting the Faria paper, I shall in this section use the modern names for these cities, even though I believe that it would have been more appropriate to have used the former names in a passage like this, which is describing the colonial era.] In a key sentence, the authors propose that “[The pandemic HIV-1 virus] arrived first at the three largest population centres – Brazzaville, Lubumbashi and Mbuji-Mayi – that were better connected to Kinshasa, indicating a critical role for mobility networks in the early spread and establishment of HIV-1 from its epicentre”. This statement is wrong on two grounds.
Firstly, throughout the colonial era Kisangani (formerly Stanleyville) had a considerably larger population than Mbuji-Mayi (once called Bakwanga). For instance in 1956, the former city, with a population of 59,000, had over four times the population of the latter (14,600). Mbuji Mayi later grew massively in population and eventually overtook Kisangani, but this was only many years after Independence.
Secondly, the colonial transport links between Kinshasa and Kisangani were considerably better than those between Kinshasa and both Lubumbashi and, especially, Mbuji-Mayi. This is because all transport along the latter route had to begin with a 6-day upstream journey by river ferry, of which there was only one a fortnight, even by the 1950s. Only at the town of Ilebo (Port Francqui) did the railway network to Lubumbashi (Elisabethville) take over. However, it was 400 miles from Ilebo to Mbuji Mayi, only 240 miles of which could be travelled by railway; the rest had to be travelled by road. There was thus no easy transport link between Kinshasa and Mbuji Mayi in the colonial era. By contrast, there was one ferry a week (allegedly often carrying over 1,000 people) that plied between Kinshasa and Kisangani, a 7-day journey when travelling upstream. Thus the central tenet of Faria’s phylogeographical argument about internal HIV-1 spread within the Congo falls apart. (I believe the inaccuracies come about through a lack of familiarity with Africa. My information comes from the 1956 edition of the “Traveller’s Guide to the Belgian Congo and the Ruanda-Urundi”. Theirs, I believe, is derived from on-line searches and Google.)
6) In an article about the Faria paper by Guardian science editor Ian Sample (“HIV pandemic originated in Kinshasa in the 1920s, say scientists”, an article about which there is more to say below), Oliver Pybus is extensively quoted. “For an epidemic like HIV where we’re trying to track back to before it was even discovered, genetics is the only source of information we have”, he says. But Pybus is incorrect, for the “dog that didn’t bark” (the complete lack of evidence of HIV-1 and AIDS prior to 1959) is another significant source of information, one that he chooses to ignore. What Oliver Pybus and his colleagues fail to make clear is that their claims to have reconstructed the early history of HIV-1 are no more than speculations, based on a very specific (and inadequate) phylogenetic model, and in the case of the historico-geographical analysis, some very poor data. Yet their observations about the mooted arrivals of HIV in these cities and towns are reported in the Science paper (and in most of the newspaper coverage) as if they were facts. They are most definitely not facts. They are speculations, with no supporting evidence, which are largely based on the preselection of HIV-1 samples from 1985 to 2004 that have been used in the geneticists’ calculations. I repeat: there is not one jot of hard evidence indicating that these speculations might be true.
7) Let’s leave the speculations to the members of the bushmeat group, and instead let’s focus on some empirical facts. In reality, the only two hard pieces of evidence for the existence of HIV-1 in the world prior to the Independence of the Belgian Congo are these: one ancient HIV-1-infected blood sample from 1959, and another HIV-1-infected sample from 1960, both coming from the Congolese capital of Leopoldville. These were samples taken two years and three years, respectively, after the first mass-trials of an experimental OPV called CHAT in the country, and 1 and 2 years after the start of the mass-vaccination with CHAT of all of Leopoldville’s children up to and including the age of four. That isn’t proven causation. It’s merely a very good clue. As is the fact that the earliest evidence of HIV-1 and AIDS in the world correlates to a highly significant degree with the venues of the OPV trials in 1957-60; (see note 9, below). As is the evidence (see above) that CHAT vaccine (a live virus that was treated with antibiotics to prevent bacterial contamination, but was not otherwise denatured) was prepared locally in the cells of chimpanzees.
8) The Faria article announces, to great fanfare, that they have proved the HIV-1 pandemic began in Kinshasa (Leopoldville). It says that others had previously proposed that it might have begun in Brazzaville or Pointe Noire, but when one checks the references, the “others” are shown to be Jacques Pepin, one of their own co-authors! They have thus set up a paper tiger and then shot it down in flames.
9) So here’s the real epidemiology, based on hard evidence, not computer-generated speculation. The OPV hypothesis agrees that the Faria analysis insofar as the major introductory point of HIV-1 was indeed Leopoldville/Kinshasa. That’s fairly obvious when one looks at the multiple evidence of early HIV-1 and AIDS in that city from 1959 onwards, as summarised in The River, pages 740-748. But apart from this evidence from Leopoldville/ KInshasa, there is also powerful evidence of either the virus (HIV-1) or the disease (AIDS) emerging in several other cities, towns and villages that were once part of Belgium’s colonial holdings: Lisala (1962); Likasi (1975); Yambuku/Abumonbazi (2 villages that are some 50 miles apart in northern Equateur province) and Bujumbura, Burundi in 1976; Kisangani and Kigali (Rwanda) in 1977; Uvira and Lubumbashi in 1978. [Because this is describing post-1960 events, I have used the modern names. Most of this information is from pages 740-748 of “The River”, save for Likasi 1975 [River, page 263], and Bujumbura 1976, which is the result of recent research.] As I say, all of these reports are supported by hard evidence (either the proven finding of HIV-1 in stored blood or tissues, or else AIDS cases that have been confirmed by physicians). For comparison, the first retrospectively recognised HIV-1 infection in the US occurred in 1977 and the first AIDS case in 1978, for the mooted 1969 case from St Louis, Robert R, is probably sprurious; [River, page 778]. But getting back to Africa, all but Likasi and Lubumbashi are either the sites of 1950s OPV trials, or else close to same (Kigali is 50 miles from a vaccination site; Yambuku 90 miles and Abumonbazi 140 miles). Initially I thought that there might also have been one vaccine trial in Shaba (formerly Katanga), the mining region that includes Likasi and Lubumbashi; (such a trial was mentioned at a 1959 press conference that was co-hosted by one of the vaccine-makers, Stanley Plotkin). But despite finding clues, I have not found evidence that this trial was ever staged. However, so many young men from vaccinated areas were recruited to the mines that it is not hard to explain the early presence of HIV-1 in Likasi and Lubumbashi.
10) The bushmeat believers seem to know little or nothing about the early epidemiology of HIV-1 in Africa. For instance, people like Worobey, Hahn and a long-time Hahn collaborator, Paul Sharp, have long proposed that there must have been “thousands” of HIV-infected people in Africa by 1960. They had to believe this, because if you work out the basic mathematics, then a constant doubling rate for the HIV-1-infected population would have reached a figure of roughly 1,450 to 2,450 HIV-infected persons by 1960, depending on whether you start your calculations from 1920 or 1908. (The end-point of their calculations is 1976, as is explained more fully in the analysis below.)
The previous claim by these bushmeat advocates that “thousands” were already HIV-1-infected by 1960 was always far-fetched, if only because this would have meant hundreds of AIDS cases occurring in the capital during the 1950s. Some, at least, would have been picked up and reported by the many capable physicians then working in Leopoldville. Yet not a single plausible case of AIDS was reported (even retrospectively) in the literature for the years up to Independence in 1960. [Pybus’s claims that ancient AIDS cases would have been merely diagnosed as TB or some similar disease, are feeble in the extreme. Most AIDS cases in Africa present with a tell-tale cluster of indicator diseases, such as untreatable bacterial and enteric infections, oral and oesophageal thrush, Pneumocystis carinii pneumonia (PCP), untreatable cytomegalovirus (CMV) infections, untreatable herpes infections, Kaposi’s sarcoma (KS) and yes: tuberculosis too. I personally interviewed many Belgian doctors who served in the Congo both before and after Independence, and not one of them mentioned a plausible colonial-era AIDS case.]
As I explained in The River [pages 259-262], the first plausible AIDS case in the medical literature is one that was reported by Jean Sonnet and Jean-Louis Michaux in 1987. [Scand. J. Inf. Dis.; 1987; 19; 511-517.] I later followed up the case using the original patient notes, provided for me by Dr Sonnet shortly before his untimely death in 1992. The patient was one “Helene”, a 40 or 50-year-old Congolese woman from Lisala, two-thirds of the way up the Congo river between Leopoldville and Stanleyville. Helene came down to Leopoldville at the start of 1962. She was admitted to hospital in February, by which time she had classic symptoms of African AIDS (including fever, malaise, thrush, multiple untreatable bacterial infections and disseminated visceral KS), and she died 12 days later. The entire population of Lisala had previously been vaccinated with CHAT, the experimental OPV, in the late 1950s, by Gaston Ninane; [River, pages 274 and 568]. The precise date is not known, but various clues indicate that it might well have been one of the first mass-vaccinations, undertaken in 1957. In another paper in which Sonnet and Michaux reported this patient as a case of AIDS, they also reported another case of fatal but uncomplicated KS from 1960, and explained why the latter had not been a case of AIDS; [River, chapter 19, footnote 5].
11) The fact that the bushmeat group has long been insisting that “thousands” of Africans had been infected with HIV-1 by 1960 is important, for it strongly suggests that for the last 15 years or so their calculations have been all wrong. They just haven’t tallied.
In the Faria paper they attempt to address this problem. They do this in an interesting way, for the authors propose that pandemic HIV-1 (or HIV-1 Group M, as they call it) suddenly and dramatically accelerated its rate of spread after 1960. They report in the text of the paper that the pandemic HIV-1 growth rate “nearly tripled” for the 1960-1976 period, compared to the initial growth rate of 1920-1960. Their data reveals that they are arguing that between 1920 and 1960, HIV-1 growth was “relatively slow”, with a growth rate of 0.1 per year (95% Confidence Intervals: 0.064 to 0.15 per year), and that between 1960 and 1976, the HIV-1 growth rate rose dramatically to 0.27 per year (95% Confidence Intervals: 0.20 to 0.33 per year). For those who want to do the calculations, remember that these growth rates are calculated using continuous compounding, which is rather like using calculus to work out compound interest.
However, if one uses these data to calculate the global population of HIV-1-infected persons in particular years, one arrives at some very interesting figures. The initially slow growth rate of 0.1 per year for 40 years would produce a total of just 54.6 infectees by 1960, and then using the higher growth rate of 0.27 per year this would produce a grand total of 4,105 HIV-1 infectees in 1976.
There is a nice way to check this Faria figure of 4,105 persons HIV-1-infected persons in 1976. All parties agree that Leopoldville/Kinshasa is the key city in the early AIDS epidemic. The bushmeat people say it was the epicentre of pandemic HIV-1 (Group M), while the OPV hypothesis sees it as the place where most of the original infections occurred. So let’s do some calculations just for Kinshasa.
Good HIV-prevalence figures for apparently healthy mothers living in Leopoldville/Kinshasa are available for Kinshasa for 1970 (0.25%) and 1980 (3.0%) [see River, page 99], and one can therefore calculate that 1.11% of apparently healthy mothers living in Leopoldville/Kinshasa would have been HIV-positive in 1976. (We may safely assume that apparently healthy mothers would have been representative of the entire city population. The disparity, if any, would not have been a large one.)
Interestingly, the only other place in the world for which there is a serological study indicating that HIV-1 was present in 1976 is Yambuku, in the Equateur province of the DRC. If that name is familiar, it is probably because this was the village which experienced one of the first two outbreaks in the world of Ebola virus in 1976. 659 blood samples that were taken for Ebola studies in 1976 were later retrospectively tested for HIV-1, and 5 (or 0.82%) were found to be HIV-1-positive. [River, pages 95-96.] The bushmeat people would have us believe that this is evidence of early HIV-1 spread out of Kinshasa. The OPV hypothesis, however, points to the 1950s OPV vaccination of the entire population of Lisala, just 90 miles to the south, and connected by a murram road that is the major transport route to the Central African Republic. (There is also documentary evidence suggesting that Yambuku itself may have been OPV vaccinated in the late 1950s, but I am still awaiting further information on this.)
But back to Kinshasa. In 1976 the population of Kinshasa was apparently 2,443.900 [See Jan Lahmeyer’s “Population Statistics” web-site: http://www.populstat.info/Africa/congokip.htm ]. So if 1.11% of that total had HIV-1 infection by 1976, this means that 27,127 persons were by then infected in Leopoldville/Kinshasa alone. That is over six times more than the 4,105 HIV-1-infected people in 1976 (in the whole world!) that are calculated using the growth rates in the Faria paper.
In short, the Faria analysis, like previous analyses by the bushmeat people, is flawed. Their growth rates are too low to explain the recorded prevalence of HIV-1 in 1976.
To make the figures tally, one would have to increase the Faria growth rates (both the 1920-60 and the 1960-76 rates) by 22.7%. This would produce an infected population of 135.4 persons in 1960, and of 27,143 persons in 1976. But an increase of 22.7% would take us fractionally outside Faria’s stated 95% Confidence Interval range for 1960-76. To bring us back within that CI range, let us increase the growth rate by slightly less – by 22.4%. This would produce an infected population of 133.8 in 1960, and 26,477 in 1976. (The latter figure is about 2.5% less than the anticipated total of 27,143 HIV-1-infected persons, but is still well within the acceptable range from a statistical perspective.)
In fact, Faria et al would need to increase those growth rates even more, for by 1976 the virus was no longer restricted to Kinshasa, but was also present in other places such as Yambuku, Abumonbazi, Likasi and Bujumbura (see note 9, above).
The other really interesting aspects of the Faria analysis are those 1960 figures for persons with HIV-1 infection, which are very much smaller than the “thousands” proposed by Hahn, Sharp and Worobey. The results of our analysis (on which I have had tremendous assistance from two “trusted advisers”, both of whom are better-versed than I in the ways of higher mathematics, especially calculus) reveal that the 1960 total of HIV-infected persons would have been 54, using Faria’s figures, or 133, using our adapted version of Faria’s figures, with its 22.7% increase in the mooted growth rates.
12) So, a remarkable detail is revealed, one that for some strange reason the Faria authors neglect to mention. If one employs the growth rates argues by Faria’s group, one finds that 54 people would have been infected with HIV-1 globally on the day that the Belgian Congo became the independent DRC on June 30th, 1960, the majority of whom would have been living in the Congolese capital, Leopoldville. And even if one adapts the growth rates upwards by 22.7%, as I believe one needs to do, the 1960 total of HIV-infected persons is still only 133.
At this point, why does the increase of growth of the pandemic AIDS virus suddenly “nearly triple”? Faria et al. state blandly: “Group M viruses expanded geographically and established new subpopulations around 1960.” It’s noteworthy that the charts and figures published in the Faria paper also reveal that the various subtypes of HIV-1 Group M also began to appear at around this same date of 1960. So what might have caused this dramatic increase in geographical spread and transmission rates from 1960 onwards? The authors have to admit the likelihood that “early HIV spread contained an iatrogenic component” (meaning that physicians themselves were involved), even if they go on to claim that this was probably as a result of “unsterilised injections at sexually transmitted disease clinics in the 1950s”. This is a favourite idea of Joao Sousa (mainly, I suspect, because it overlaps time-wise with the much likelier source, namely the OPV trials).
The OPV hypothesis, of course, would point to the OPV trials staged in the late 1950s in places such as Leopoldville/Kinshasa, Lisala, Stanleyville/Kisangani, and Usumbura/Bujumbura. Only Jadotville/Likasi (of places where HIV-1 had already arrived by 1976) falls outside this range, and it is entirely possible that HIV-1 infection in Likasi was seeded by the importation to Katanga, the mining region, of labourers from OPV-vaccinated towns such as Usumbura. (As I recall, over a fifth of the Katanga mining population was brought in from Ruanda-Urundi, of which Usumbura was the capital.) It is also possible that the Belgian who fell sick with symptoms of AIDS in Likasi in 1975 was actually infected elsewhere, such as Kinshasa, which he would certainly have visited while travelling back to Belgium on holiday, which would have happened several times between 1964 and 1977, the year of his death.) [River, pager 263.]
So, to sum up, the bushmeat believers, after blaming an African hunter or bushmeat-seller for the initial viral transfer from chimpanzee to human, are now effectively blaming unnamed workers at STD clinics in Leopoldville in the 1950s for accelerating the spread of HIV-1 just before Independence. This of course conveniently absolves the Belgian and American vaccine-makers (some of whom, like Stanley Plotkin, are still alive) of any responsibility. This also conveniently avoids the enormous and enormously embarrassing political implications of the OPV hypothesis.
13) But this approach is also quite clever, for if the OPV hypothesis ever comes to be accepted (as I am confident it eventually will be, despite the bushmeat shenanigans of the last 15 years), then its proponents can still try to rescue, or part-rescue, their moribund hypothesis by saying: “Look: we told you it was all about iatrogenic events in the 1950s. They were just different events from the ones we proposed!” The truth, however, is that the entire history of HIV-1 that they present up to 1959 is false. It is nothing more than a fantasy created by people whose inner convictions (the concept of TMRCA, and the use of a mutational model to analyse a virus that mainly evolves in a different way, through recombination) mean that they must hypothesise an earlier hidden epidemic, even if there is not one single shred of evidence of HIV or AIDS from before 1959 to support it.
14) But here’s the kicker. We now have a major paper from the bushmeat origin school which clearly provides dramatic support to the OPV hypothesis in its analysis from the late fifties onwards. The reason I make this claim is that for some years now I (and other OPV proponents) have been saying that the likeliest number of persons to have been infected due to the OPV trials staged up to and including 1960 could only be broadly estimated, but would probably be within the ranges of 10-1,000. (My gut feeling, on the basis of the early epidemiology of HIV-1 and AIDS, a subject that I have been researching since 1990, was that around 100 people would have been initially infected with slightly different versions of the ancestral pandemic HIV-1 virus, these being acquired via different batches of the living OPV that was locally prepared in chimpanzee cells, and then administered to roughly a million people. However, this was only a guess, albeit an informed guess, and I was aware that it needed to be underpinned by wide probability levels, probably involving an order of magnitude on either side, in other words 10-1,000. Other supporters of the OPV hypothesis concurred with this.)
So the bushmeat group’s latest analysis, and its conclusions about the number of HIV-infected persons in 1960 (54 to 133) strongly aligns with the number forecast by the OPV hypothesis. Not only does it align with that number, but it matches it to a quite striking degree. The only difference is that the OPV hypothesis proposes that these 54 to 133 persons were infected by an experimental vaccine, not by an imagined chain of infection starting in south-eastern Cameroon in 1908, or Leopoldville in 1920, or wherever and whenever. And that, I suspect, is why that small but pertinent detail (the figure of 54 to 133 persons infected in 1960) was for some reason left out of the Faria paper in Science.
15) Another way of putting this is that if the bushmeat geneticists were to do what they have always refused to do (despite my asking them) and to use their phylogenetic clocks to estimate a punctuated event (such as a flawed vaccination campaign in 1957-60) instead of a single transfer in 1908, 1920 or whatever, they would end up with 133 infectees in 1960 (via the punctuated event, namely the various OPV trials), and arrive at the exact same outcome in 1976: 27,000-odd infectees in Leopoldville/Kinshasa, and the beginnings of a pandemic that would go on to kill 40 million or more persons. The analysis in the Faria paper proves it.
So let me thank these authors. Their analysis provides the data that the bushmeat hypothesisers have always refused to provide previously. After years of spurious and misleading science, the bushmeat scientists have finally got something right. The next step would be for them to admit that their claims of an earlier epidemic in the years up to the 1950s are not supported by one shred of hard evidence. But given the certainties of the people involved, I’m not expecting any admissions of error, or even of shortcomings, any time soon.
16) Finally, I have to report an example of a particularly misguided and deplorable form of media censorship, by none other than the much-respected Guardian newspaper, for which I contributed articles from Africa for three years in the mid-1980s, and which has always been my own newspaper of choice, not least because of its recent fine coverage of the Snowden and Assange stories. The Faria paper was covered by an uncritical article by the paper’s Science Editor, Ian Sample, entitled “HIV pandemic originated in Kinshasa in the 1920s, say scientists”. Comments were invited on the Guardian web-site. I scanned through and noticed that one person, “Worried”, had posted a comment saying: “I would like the Guardian to ask the author of THE RIVER to reply to this ATL. As far as I know he is the only person qualified to do so.”
Although I was heading out an hour later, I quickly penned a comment just under the word limit, and posted it on the site. When I got back 3 hours later, I found that my comment had been removed, with a note saying that it was in a state of “pre-moderation” which, as was later made clear, was tantamount to being transferred to a state of limbo. I was now referred to only as “ID4556018”. The initial comment by “Worried” had now also been removed by a community moderator. Two other mildly-phrased comments that were supportive of the OPV hypothesis by one Tom Holzinger had been removed as well. (I know this because Holzinger emailed me via the web-site after posting his comments. He was completely shocked when they were subsequently taken down. Holzinger, by the way, is the only person who made comments on the Guardian web-page whom I know, and then only through email contact.)
Another reader who had obviously seen my web-site comment before it was removed had left the following comment: “Could you please explain how exactly the highly interesting and relevant post from ID4556018 posed a problem?” Of course, this meant nothing to those who did not know what had been written by ID4556018. All this was intriguing, for it was now clear that pro-OPV comments were being removed by the team of community moderators. (Many other comments had also been removed by the moderators, but it is not known how many, if any, of these might have been supportive of the OPV hypothesis. Yet two rancid examples of racism and sexism were left untouched, merely because they had included an asterisk in the middle of the more offensive words.)
It seemed clear that the moderators were exceeding their official remit as protectors of community standards, and were acting instead as censors in a scientific debate. (By contrast, when the New York Times wrote about a paper by Michael Worobey that featured his highly contentious claim that he had proved with 99.8% certainty that the US epidemic of AIDS had started with the introduction of a single virus from Haiti, the web-site comments included more entries that were supportive of the OPV hypothesis and myself than of Worobey and his phylogenetic dating approach. This was despite the fact that neither the OPV hypothesis nor my name had been mentioned in the original article. The NYT web-site, at least, was apparently not censored.)
I wondered whether Ian Sample, the Guardian Science Editor, or any of the authors of the Faria paper might have been involved with the community moderation process. I therefore wrote a letter reporting what had happened and explaining my concerns. I emailed it to the Guardian team of community moderators, asking them to reconsider their position, and in any case asking them to explain why the pro-OPV comments had been taken down. I waited 3 days and got no response.
I then wrote a letter to Chris Elliott, the Guardian readers’ editor, a sort of internal ombudsman for the newspaper, again explaining my concerns. It was over the 500-word limit that one learns (as one is about to send one’s email) is supposed to apply, but (as I explained in a postscript email) I felt that the situation was so grave that it could only be explained properly in a greater number of words. 12 days have passed, and again, the silence is deafening.
The only thing that has happened is that after a week, by which time the web-site had closed and was no longer deemed newsworthy, one of Holzinger’s posts was put back up by the moderators. The news was conveyed to Holzinger in what struck me as a sanctimonious email, which pointed out that in future he would need to respect the fact that nobody is allowed to discuss the moderators’ decisions on line. (He had apparently done this in a follow-up posting to his two initial comments.)
The real purpose of this about-face on Holzinger may well have been to allow the moderators to argue that they had not been inherently biased against the OPV hypothesis. I, however, believe there is prima facie evidence indicating that they have been prejudiced, and shamefully so. Sorry, Guardian, but I’ve waited almost three weeks for an explanation, and none has come. In any case, in a debate such as this, one can’t afford to have favourites.
Conclusion
The geneticists and medical historians who collaborated on the Faria paper in Science employed a faulty model for HIV-1 dating (a so-called molecular clock which ignores the possibility of a punctuated event) and a biased preselection of HIV-1 samples, giving conveniently misleading results which they have readily adopted because they seem to tally with their own preconceived views. But over and above this, their analysis in the paper, including both the HIV-1 growth forecasts and the historico-geographical analysis, is also flawed.
I sent an early draft of this set of notes to several people whose judgement I respect, seeking their comments and their thoughts on the Faria paper. One of them – a man I have known for over 20 years, who has always retained an open mind about the origins debate, made the following comment: “the real problem with the [Faria paper is that] there are no new data! All the rest is modelling (meddling) and politics.” He pointed out that only the finding of an HIV-1 sample from before the time of the OPV trials would provide any degree of evidence for the bushmeat argument. But researchers have been searching freezers and pathology departments for 29 years, since the 1985 discovery and reporting of the 1959 sample, and nothing earlier has ever been found. As I have been saying for the last decade, if there should suddenly be an amazing discovery of a sample of HIV-1 from the first half of the 20th century, then this would be mighty convenient for the members of the bushmeat school. One wonders how they would seek to prove that such a sample was genuinely from before 1950, and not a sample from, say, 1958 or 1960, that had somehow come to be mislabelled.
I was also pleased to hear from a European doctor who has had a privileged position near the heart of the origins debate for 15 or more years. He cannot be identified, but he knows a great deal about what has really gone on in the background. A few days ago he called me. When I asked if he had seen the Faria paper in Science, he said that he had, and that it was “shameful”. He expressed his anger about the shoddy work, and went on: “It’s not worthy for an institution of science like Leuven. These people are not doing science. They’re doing politics.” I have heard from more than a dozen people, all indignant, and all quite clear that the paper is deficient in value. It’s good to know that not all the world is so easily fooled.
Let me also quote some words from one of the authors of the Faria paper, Joao Sousa, with whom I have engaged in a civil, but adversarial email correspondence over the last decade or so. Sousa recently emailed me a copy of the paper of which he is a proud co-author, and commented that the analysis in the article is “a masterpiece”, and that Beatrice Hahn and Michael Worobey think that the work is “brilliant”.
I cannot agree, although for the reasons stated above I have found good use for some of the research, if not for the analysis offered by the authors.
I’d like to close by highlighting the role of the “trusted advisers” from various fields of science and the humanities who have read and made helpful comments and/or corrections on an earlier draft of this paper. All of the posts on this web-site are similarly checked and reviewed by experts in different fields before they are published. Though they cannot be identified by name (lest they be vilified as “subversives” or “conspiracy theorists” by those who insist that the bushmeat hypothesis is proven) I’d like to thank these advisers for their good judgement, their generosity and their time.
Ed Hooper October 23rd, 2014