More supportive of OPV/AIDS than of the bushmeat hypothesis. (A revised response to the recent Faria paper in Science.)

[A recent communication from one of the co-authors of the Faria paper has provided new information, which requires an updated response from myself. Surprisingly, this information reveals even more evidence in favour of the OPV theory. Ed Hooper, November 11th, 2014.]

Several people have recently asked (either via the AIDSorigins 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 on-line earlier, it was 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 some of the previous problem areas in their work, and certain crucial aspects of their analysis, though they do not advertise it, now align very closely with what I have been proposing for several years. 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 locally in Africa in the cells of common chimpanzees.

Many readers of my book The River (Little, Brown/ 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 virus that caused the AIDS pandemic, HIV-1 Group M, emerged from south-eastern Cameroon early in the 20th century (their major estimates have been, in chronological order: the 1940s or early 1950s; 1931; 1908 and now 1920), 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 hypothesis 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 scientific investigation.

Let me be very clear about this. It is a scientific error to assert that one hypothesis disproves another hypothesis, as the bushmeat proponents have been doing for over ten years now. The bushmeat gang have no facts to disprove the OPV hypothesis, only their own hypotheses. They are not engaging in scientific debate. I do not claim that the OPV hypothesis proves them wrong. What I claim is that the known facts are consistent with the OPV hypothesis, and no facts have been shown to refute it, despite the bushmeat claims. The bushmeat refusal to acknowledge this (just like the unwarranted promotion of their claims by Nature and Science) undermines both the philosophy and ethics 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 key flaw in the paper is that the authors of this article, like other bushmeat authors before them, assume that the AIDS pandemic began with a single viral transfer from chimpanzee to human. This is speculation, though the bushmeat scientists treat it as if it were proven. Their assumption subsequently forces them 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 [see below], they have inadvertently produced evidence that favours the OPV hypothesis far more than the bushmeat hypothesis of origin.

2) Faria et al. hypothesise that HIV-1 began in Leopoldville, Belgian Congo in the year 1920. (They actually call Leopoldville “Kinshasa”, though the city 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.)

This seemingly bland statement actually conceals a tectonic shift in the bushmeat group’s thinking about how to analyse the AIDS pandemic. Although the Faria group makes it clear that they believe that “the cross-species transmission of [chimpanzee] SIV to humans…probably occurred in southeast Cameroon”, they make no mention of Michael Worobey’s mooted crossover date of 1908. There is no admission of a major change of approach. But although previously the common ancestor [or MRCA: see below] of HIV-1 Group M was assumed to coincide with the mooted chimp-to-human transfer, it is now assumed to post-date that transfer, and to coincide with the beginnings of viral spread in a major city.

The authors write: “After localised transmission, presumably resulting from the hunting of primates, the virus probably traveled via ferry along the Sangha river system to Kinshasa. During the period of German colonisation of Cameroon (1884-1916), fluvial connections between southern Cameroon and Kinshasa were frequent due to the exploitation of rubber and ivory.”

Having thus disposed of a 550-mile gap, the authors apparently forget that they have been speculating (as revealed by their use of the words “presumably” and “probably”), for their next sentence reads: “With the geographic origins of pandemic group M clear, we next sought to investigate its spread from Kinshasa to the rest of Africa.”

Actually their change of thinking about the origins of pandemic group M is anything but clear. But the authors gloss over this and roll onwards, asserting that their phylogenetic “analyses robustly place the spatial origin of the HIV-1 Group M pandemic in Kinshasa”. They add that: “In line with previous approaches, we estimated that the time of the most recent common ancestor (TMRCA) was around 1920.”

But I repeat: the authors give no explanation as to why they have apparently abandoned a 1908 start-date for the epidemic in Cameroon for a 1920 start-date in Leopoldville/Kinshasa. This gives the impression that they are trying to have their cake and eat it, as we say in England. (If this is unclear, it means “trying to keep the cake, but also eat the cake”.)

But in real life, you can’t have it both ways. Either the 1908 claim is correct, in which case there would be several strains of HIV-1 in existence by 1920, not just one single ancestral strain. Or else the 1920 claim is correct, in which case they need to explain why they are rejecting the 1908 scenario. They can’t just hedge their bets and imply that they believe in both versions.

(As an aside, the main selling point of the Faria article was its announcement, to great fanfare, that its authors had proved that the HIV-1 pandemic began in Kinshasa/ Leopoldville. It claims that others had previously proposed that the pandemic 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.)

3) In any case, I strongly dispute the claim by Faria et al. 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.

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 the Faria 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.

4) But as briefly mentioned in point (1), their molecular dating analysis is also flawed in another major way. Without any supporting evidence, the bushmeat scientists have for many years been insisting that there was a single source for the pandemic. They have assumed that humans initially acquired HIV-1 through a single event: the crossover (from a single chimp to a single human) of a Simian Immunodeficiency Virus (SIV) which is found in common chimpanzees (Pan troglodytes), and which is acknowledged as the closest ancestor to pandemic HIV-1. Without any supporting evidence, the bushmeat scientists assume that this viral crossover led to the infection of one human index case, which they like to refer to as the “Most Recent Common Ancestor”, or MRCA. But the very concept of an MRCA for HIV-1 is in itself highly controversial.

Superficially the work 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 slightly different 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.]

5) 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) by 1946 and Kisangani (then called Stanleyville) by 1953. It also reports that HIV-1 crossed the river from Leopoldville to what is now often colloquially called “Congo-Brazzaville”, to reach the city of Brazzaville in 1937 and the port of Pointe Noire a few years later.

We thus have to assume that the bushmeat clan is now proposing that the initial HIV-1 virus originated at some unknown earlier time (possibly 1908; possibly not) in Cameroon, and then travelled down from Cameroon through Congo-Brazzaville (a modern colloquial name for what in those days was the territory of Middle Congo in French Equatorial Africa) to Leopoldville in the Belgian Congo in around 1920 and then, 17 years later, crossed back over to Congo-Brazzaville again to infect Brazzaville in 1937 and then move on down to the coast. Such are the convolutions required by the bushmeat hypothesis! There is no data to support any of this. But it provides a pretty map to show in the paper.

What it leads me to suspect is that they have discovered that some of the basic tenets of their theory are weak, or simply wrong. And they are desperately trying to reposition themselves.

6) However, there are also major errors in their historical analyses. [Since I am quoting the Faria paper, I shall in this section use the modern names for these cities.] 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 (formerly 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 in the 1950s. Only at the town of Ilebo (ex-Port Francqui) did the railway network to Lubumbashi (Elisabethville) take over. However, it was 400 miles from Ilebo to Mbuji Mayi, and only 240 miles of this 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 partly because of 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 largely from on-line searches and Google.)

7) 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.

8) Let’s leave the speculations to the members of the bushmeat group, and instead let’s focus on some facts. The key fact is that the empirical history of HIV-1 and AIDS goes back only as far as 1959.

In reality, the only two pieces of hard 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 in the Belgian Congo of an experimental OPV called CHAT, and one and two 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 presented above, that CHAT vaccine (a live virus that was treated with antibiotics to prevent bacterial contamination, but was not otherwise denatured to control adventitious viruses) was prepared locally in the cells of chimpanzees.

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 spurious; [River, page 778].

Thus all the places where HIV or AIDS was detected between 1959 and 1978 (save for 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. (To tie in with the Faria analysis, I have used the year 1976 as an end-point, 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 (TB) 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 pertains to 1962, and 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 “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, lymphadenopathy, respiratory infections, multiple untreatable bacterial infections of the skin, mouth and throat and disseminated visceral KS); 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. Faria et al. claim that there was “a stabilisation of epidemic growth” after 1976, and claim “that this slowdown agrees with reports of relatively stable HIV prevalence in the DRC from 1976 to 1997”. My own research indicates that HIV-1 prevalence in the DRC became fairly stable about a decade later, in about 1986, but for the purposes of the present analysis let us accept the Faria interpretation, and use 1976 as an end-point.

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 exponential growth, which is like using calculus to work out continuously compounding 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, in 1976, experienced one of the first two outbreaks in the world of Ebola virus. 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 – to a small village about 800 miles away in the bush. 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 from the River Congo to the Central African Republic. (There is also documentary evidence suggesting that Yambuku itself may have been vaccinated with OPV 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]. So if 1.11% of that total had HIV-1 infection by 1976, this means that some 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.

12) Since posting the initial version of this paper on October 24th 2014, I emailed one of the co-authors of the Faria paper, Joao Sousa, to ask if he could help explain this apparent discrepancy. He emailed back to say that he is no phylogeneticist, but that based on discussions and email communications with his co-authors, he understands that what their paper is measuring is the “effective population size” of persons with HIV-1, which is represented by the “Ne” symbol. He writes: “I understand that Ne (the effective population size) grossly underestimates the [total] number of infectees. The Ne more or less attempts to measure the number of infections that lead to long term progeny. So the fact that the Ne calculated by [Faria] and colleagues is close to 100-200 in 1960 does not preclude the existence of thousands of infectees by then. Simply, most infectees do not transmit [HIV to others], and so they don’t contribute to Ne.” (He goes on to argue that if two samples of HIV-1 were detected in Leopoldville/Kinshasa in 1959 and 1960, this means that there must have been thousands of infectees by 1960 in that city alone. I find this a very weak argument, based on nothing more than speculation, and believe that it is outweighed by my argument above, that thousands of HIV infections by 1960 would have meant hundreds of AIDS cases before 1960, yet not one case was actually identified by the large team of experienced doctors then working in that city.)

Yet none of this crucial discussion (the difference between Ne, the “effective population size” of HIV-1 Group M infectees, and the true number of persons infected with HIV-1 Group M in any particular year) features anywhere in the Faria paper, and most readers of the paper would have no idea that its authors are proposing that the true number of HIV-1 infectees in any particular year is many times larger than the “effective population size” that is discussed in the paper. This is clearly yet another significant flaw in the paper.

Moreover, it shows that once again, when one presses the bushmeat authors on the precise details of their scientific techniques, it becomes apparent that the explanations offered in their papers are often inadequate.

So let us try to reconcile the known data about the size of the HIV-1(M) epidemic in 1976 with what is reported in the Faria paper. To repeat, if HIV-1 Group M grows exponentially at 10% per year from a figure of 1 in 1920, then it gets to 54 in 1960, and if it grows at 27% thereafter, then it reaches 4,098 by 1976. But my epidemiologically-supported figure for 1976 is 27,127 Group M infectees. If we once again employ the Faria growth rates and work backwards in time from that 27,127 in 1976, then we arrive at 361 infectees in 1960, and between 6 and 7 infectees in 1920. It would seem, therefore, that the Faria group believes that HIV-1 Group M’s “effective population size” is one out of every 6 or 7 infected persons, or roughly 15% of the total number of Group M infectees.

But note that figure for 1960, of just 361 people. In the Faria paper, they state that “HIV-1 was largely restricted to Kinshasa for most of [the] period…between 1920 and 1960”. It is therefore clear that their 1960 figure for Group M infectees is considerably less than the “thousands” that Sousa, Hahn and Sharp all insist were infected by then. Once again, their sums don’t support their claims.

They do, however, support the OPV theory. 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, with its unrevealed conclusions about the number of HIV-1 Group M-infected persons in 1960 (be it an “effective population size” of 54, or a total number of Group M infectees of 361) strongly aligns with the number forecast by the OPV hypothesis. The only difference is that the OPV hypothesis proposes that these 54 to 361 persons were infected by an experimental vaccine, rather than 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 these small but pertinent details (the figure of an effective population size in 1960 of 54, and a total number of infectees in 1960 of about 361) were completely omitted from the Faria paper in Science.

It is worth emphasising that even this analysis would not have been possible without the additional information about Ne provided informally by Joao Sousa. The only information that can be deduced from the Faria paper about the number of Group M infectees in 1960 comes from the graph in Figure 4. If you examine Figure 4 very carefully, using a magnifying glass, it shows, after accounting for the log scale on the vertical axis, a value of about 190 for a compound variable that they call “effective infections” [Ne] times “mean viral generation time” [tao]. Surprisingly, neither of these terms is defined in the paper. If Ne is the “effective population size” of Group M carriers (ie the number of infectees who later transmit infection to others), then the left-hand scale is still effectively encrypted by the fact that no information is provided about tao – either by Faria in the paper, or by Sousa (despite my asking about it). All one can say is that if the value of tao is around 3.5 for 1960, then their numbers match up with Ne of about 54, and total Group M infections numbering about 360, as calculated above. (This speculation is merely an attempt to make sense out of the Faria numbers and their undisclosed assumptions.)

In short, the approach used by the bushmeat phylogeneticists renders their work incapable of checking by neutral observers. Figure 4 in Faria’s paper, for instance, is described as featuring “Bayesian skygrid estimates of past population dynamics for Group M”, whatever these might be. One might as well write: “Assumptions and estimates used by the bushmeat group in order to lend superficial credibility to their speculations”.

However, since the concepts and variables displayed in Figure 4 are not explained in the paper or in the on-line “Supplementary Materials”, this means that the graph is effectively encrypted, and represents a secret calculation. Just like their dubious phylogenetic dating work, the mathematical concepts invoked by the bushmeat scientists are complicated and so inadequately explained that others (such as geneticists, mathemeticians, journalists – or even, it seems from what Sousa writes, co-authors!) are unable to check them. All one needs to emphasise is that straightforward mathematical analysis reveals that there are fundamental errors in the Faria calculations.

In fact, it seems that the lack of clarity may be deliberate, and may be employed in order to allow the authors to fudge both their figures and their arguments.

13) At this point, one needs to ask why the growth rate of the pandemic AIDS virus, HIV-1 Group M, suddenly “nearly triples” in 1960. 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 around 1960? The authors have to admit the likelihood that “early HIV spread contained an iatrogenic component” (meaning that physicians themselves were at least partly responsible), 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 one branch of the bushmeat proponents, such as Jacques Pepin (mainly, I suspect, because it overlaps time-wise with the much likelier source, namely the OPV trials).

The OPV hypothesis, of course, would propose that this time frame (late 1950s up to 1960) marks the point when HIV-1 Group M arrived in Homo sapiens, not when there was a sudden exponential rise in its rate of spread. The OPV hypothesis would also point to the CHAT vaccine trials staged in the late 1950s in places such as Leopoldville/Kinshasa, Lisala, Stanleyville/Kisangani, and Usumbura/Bujumbura, as the cause. 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, in colonial times 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 during his stay in Africa from 1964 to 1977. His notes imply that after his wife returned to Belgium at the end of the 1960s he had frequent sexual encounters with Congolese women. His wife remained HIV-negative.) [River, page 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 in the early 20th century, 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 OPV-makers (some of whom, like Stanley Plotkin, are still alive) of any responsibility. It also conveniently avoids the enormous and enormously embarrassing political implications of the OPV hypothesis for the various participating institutions and governments. The bushmeat hypothesis is, above all, a convenient hypothesis.

14) 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 prior to 1959 is false. It is nothing more than a fantasy created by people whose inner convictions (the concept of an MRCA, 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 shred of evidence of HIV or AIDS from before 1959 to support it.

15) 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. It postulates that the “Group M viruses expanded geographically and established new subpopulations around 1960”, and in an attempt to explain this, it postulates that “early HIV spread contained an iatrogenic component”. (The only error here is that it was actually the first arrivals of HIV-1 in Homo sapiens which involved “an iatrogenic component”.)

It also proposes a number of HIV-1 Group M infectees in 1960 which ties in very nicely with my own guestimates of the number who were initially infected with the experimental, locally-prepared OPV called CHAT.

Though the paper by Faria et al. does not intend it, it makes significant additions to the evidence in support of the OPV/AIDS hypothesis.

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 vested interests 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 that came in 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 permanent 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 my 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, and 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. He never responded.

The only thing that has happened is that after a week, by which time the on-line comments section on Ian Sample’s article had closed because the topic 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 over a month 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.

It is ironical therefore that despite its flaws, the Faria paper actually provides substantial evidence in support of the OPV/AIDS hypothesis.

One of the first persons to email me with his thoughts on the Faria paper was a scientist whom I have known for some 15 years. He concluded his email as follows: “This paper supports an iatrogenic generation of the HIV-1 M epidemic in the late 1950s early 1960s. [Moreover, if] the chimps and people move, then their geographical focus on a Kinshasa origin is unsupported.” He went on to say that the chimp SIVs had been around in chimps for many millennia, and may occasionally have infected human hunters or butchers, but without causing chains of infection or an epidemic. “However, as the authors demonstrate, something quite quantitatively different occurred in around the late 1950s and this seems to be linked to medical procedures….Could this something that was quite different relate to OPV?” He also wrote: “I think they use the word ‘iatrogenic’ to deliberately obscure this [possibility] and they do not mention it in the abstract to avoid trouble.”

Later, I sent an early draft of this set of notes to several other people whose judgement I respect, seeking their comments and thoughts. One of them – a research scientist with a background in medicine whom I have known for over 20 years, 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. Again 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. Throughout that period, Sousa has been searching for historical data that might lend support to the dating scenarios which he believes have been proved by the bushmeat school, and particularly by the work of Beatrice Hahn, whom he clearly admires. 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 suggestions on earlier drafts of this paper. I’m especially indebted to two of these advisers, both of whom are far better-versed than I in the ways of higher mathematics, and who have contributed much to the analysis of the maths in the Faria 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 November 12th, 2014