The Origins of AIDS (30 page)

BOOK: The Origins of AIDS
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At some point between 1960 and 1966, among the 4,500 teachers dispatched to Congo-Léopoldville, a single Haitian technical assistant was infected with HIV-1 group M subtype B (
Chapter 11
). Around 1966, this person went back to Haiti and stayed long enough to start a local chain of sexual transmission
.
There, this rare subtype of HIV-1 had to be amplified exponentially early on, otherwise it would have been impossible for a virus introduced in 1966 to infect 8% of women in Port-au-Prince sixteen years later, reaching a level seen in Léopoldville–Kinshasa only several decades after its introduction
.
22

23
Did this amplification occur sexually, within the small homosexual/bisexual community of male Haitians selling sex to American tourists, as suggested by some? I doubt it very much, for a simple reason: American gay tourists did not stay in Port-au-Prince or elsewhere in Haiti for long enough. For exponential amplification to occur through the homosexual route, as documented later in San Francisco, New York and many other locations, a first HIV-infected person needs to transmit the virus to one or two individuals, then each of these second-generation cases needs to infect a few more, and each of these third-generation cases to infect a few more, and so on, with a short interval (three or four months) between each cycle of transmission. Most American tourists who acquired HIV-1 subtype B from a Haitian male prostitute probably went back to the US within a couple of weeks, before they developed the high viraemia and high infectiousness which is characteristic of primary HIV infection and which drives the sexual amplification of HIV. Thus, these tourists had little opportunity to infect a second Haitian male prostitute for such a vicious circle to be initiated but a much greater chance of infecting other American gay men back home. Some
American gay tourists undoubtedly infected Haitian male sex workers, or acquired HIV-1 from these same prostitutes, and some homosexual prostitutes infected each other, but it does not seem plausible that this caused a massive spread of the virus within the small Haitian bisexual community severe enough for the infection to spill over quickly into the heterosexual population
.
24

26
Admittedly, this part of the story remains unproven, but there are good reasons to believe that the Hemo-Caribbean plasmapheresis centre (
Chapter 12
) could have been the perfect breeding ground for a quick increase in the number of HIV-infected Haitians, to a level where sexual transmission would then inevitably but more slowly allow for its further dissemination. Extremely rapid transmission of HIV-1 was documented among individuals selling their blood in commercial plasmapheresis centres in China, Mexico and India. Once the virus is introduced among paid plasma donors, up to three-fourths can get infected within a year. It seems unlikely that the procedures that should have prevented the transmission of blood-borne viruses were more stringent in Port-au-Prince than in all these other places, quite the contrary
. Haitian plasma sellers were even poorer than their counterparts in other countries and they had to put up with whatever was done at the Hemo-Caribbean clinic. For this disaster to have happened, we need just one HIV-1-infected person to have entered the cohort of plasma sellers; within the next year, from a handful of HIV-1-infected persons on the island, there could have been several hundred. At this stage, the number of infected persons in Haiti had reached the critical mass which enabled it to disseminate successfully among sex workers, male and female, and then into the general adult population
.
If indeed this happened, then the export of the plasma to the US, where it was bought and processed by large pharmaceutical companies, could have allowed for some spread of HIV-1 subtype B into the Americas and Western Europe. Once a shipment of plasma entered the stock of a plasma broker, it could be sold and resold in several countries on both sides of the Atlantic within a short period of time (
Chapter 12
). We do not know whether all of the plasma sent to the US or Europe by
Hemo-Caribbean was processed into
albumin and
immunoglobulins (with no risk of HIV transmission), or if some lots were used to prepare factor VIII
cryoprecipitates, in which case this business could have contributed to the spread of the virus. Either through this route or via American gay tourists, HIV-1 was introduced into the US
. It
was already present, albeit at a low prevalence, among drug addicts in the mid-1970s, a population within which HIV spread quickly: by 1979, one third of addicts in
New York were
infected
.
27

28
Following the 1969 Stonewall riots, a gay rights movement emerged in the US, and San Francisco became its focal point where 5,000 homosexuals migrated each year, in search of freedom and tolerance. By 1978, 6% of gay men in San Francisco were HIV-infected. The same year, through some of them who donated blood, HIV entered the local blood supply. The extraordinary level of sexual promiscuity within this population, recently liberated from centuries of repression and stigmatisation, led to an exponential homosexual amplification of HIV-1. Many of the initial cohorts of HIV-1-infected gay men had 100–200 sexual partners per year, most often during anonymous encounters in bathhouses. HIV prevalence among San Francisco gay men increased to 19% in 1979, 33% in 1980 and 44% in 1981. The incidence peaked around July 1981, when 1.4% of gay men acquired HIV infection each month
.
25
,
29

31
HIV infections were identified retrospectively among American haemophiliacs starting in 1978, but the virus may have been present at a low prevalence for some years. It was already infecting some British haemophiliacs by 1979. In a cohort of American haemophiliacs, just a few with stored serum going back to 1976, the first case of HIV infection appeared in 1978, with rapid spread in 1981–2. More than half of haemophiliacs in
Georgia were HIV-infected by 1981, as were 85% of their
Californian counterparts by 1984. The first cases of AIDS among haemophiliacs were recognised in early 1982.
32

35
Thus by the late 1970s in the US several modes of HIV transmission acted concomitantly, to a large extent independently of each other but with occasional interconnections. Haemophiliacs who happened to be gay might have sexually infected other gay men and homosexually infected men might have been volunteer blood donors or paid plasma donors. This latter step diversified the sources of HIV-1 which from multiple sites now entered the complex process that led to the production of
coagulation factor concentrates made from pools of plasma collected from thousands of donors, by then hugely popular among haemophiliacs and their physicians. The all-male haemophiliacs were otherwise healthy and, if old enough, sexually active. Some infected their female spouses (who in turn could infect their infants) but, because the average number of concomitant sexual partners was low, these
became epidemiological dead ends. Although a tragedy with almost half of the 20,000 American haemophiliacs infected, this had only a modest impact on the overall picture. Whole blood
transfusions did not contribute much to the overall dissemination of the virus either, because most recipients were sick or elderly individuals undergoing heart surgery or being treated for leukaemia or some other nasty disease, who were not active sexually in the ensuing months. Furthermore, because of the massive infective dose, transfusion recipients developed AIDS and died within just a few years. HIV-1 transmission among
drug addicts was more consequential: to generate the income needed for their dope, some addicts sold sexual services or became paid plasma donors, others happened to be gay and infected their sexual partners, and female addicts could infect their offspring
.
During the 1970s, there was much dissemination of HIV by gay men visiting other cities where they had unprotected sex. The case of the Air Canada flight attendant, the so-called ‘patient zero’, who was linked to many early cases of AIDS in various American cities, has been described in detail elsewhere. Mobility and promiscuity proved excellent breeding grounds for a sexually transmitted virus, allowing exponential transmission by men who continued having sex with other gay men shortly after they developed a high viraemia during their primary HIV period. Transmission was further facilitated by the high prevalence of other sexually transmitted pathogens within the homosexual community. In this early phase of the epidemic in the US, in all risk groups combined, each HIV-infected person infected another person every year or so. From the United States, the virus was re-exported to many parts of the industrialised world
.
36
,
37
Eventually, after an incubation period of roughly ten years during which their CD4 lymphocytes were progressively destroyed, these early American patients developed a variety of opportunistic infections and a new disease was recognised by the physicians who published the landmark
MMWR
short article in 1981. And thus AIDS was born.
 
15
Epilogue:
lessons learned
 
Twenty-nine million deaths later, are there any useful lessons that can be drawn from this tragedy? Or was it just an extraordinary confluence of chance events, unlikely ever to be repeated? In retrospect, two factors probably drove the emergence of SIV
cpz
into HIV-1. Even if their respective contributions will never be fully sorted out, there is little doubt that without them the pandemic would not have developed.
The first was the profound social changes that accompanied the European colonisation of central Africa, eventually leading to sexual behaviours far different from those of traditional societies which had lived there for 2,000 years. A relatively small number of women had sex against remuneration, initially with a few regular clients, and then, after 1960, with a large number of men, a process which amplified the transmission of sexually transmitted pathogens, both the traditional ones (gonorrhoea, syphilis, etc.) and the emerging one, HIV-1. This is just another example of the complex relationships between social changes and diseases.
Tuberculosis emerged as an important cause of adult mortality in nineteenth-century Europe, when the industrial revolution brought many poor peasants to the cities where they lived in crowded, unhealthy conditions conducive to the transmission of this respiratory pathogen. More recently, in the last decades of the twentieth century, an unprecedented epidemic of obesity has developed in industrialised countries as a consequence of our sedentarisation, itself driven by the ever-increasing availability of motor vehicles, televisions, video games, the Internet, and so on. Upcoming changes in the lifestyle of future generations will impact on the incidence of various diseases, in a way which is hard to predict and which cannot be avoided. Some of these changes could be detrimental to the human race, while others will represent progress. For instance, the progressive reduction in the use of fossil fuels and their replacement by greener sources of energy should eventually lower the incidence of the respiratory diseases associated with air pollution.
The second factor in the emergence of SIV
cpz
into HIV-1 was its parenteral amplification through poorly sterilised syringes and needles, re-used on many patients. In central Africa, this may have jump-started the epidemic by increasing the number of infected humans to a level where sexual transmission could thrive. In retrospect, this iatrogenic amplification resulted from a lag of only about fifty years between the development of therapeutic agents that required their IV administration and the realisation that infectious agents, especially viruses, could be transmitted by this route. When humans manipulate nature in a way that they do not fully understand, there is always a possibility that something unpredictable will occur.
This is a reminder that the most dangerous threat to the long-term survival of the human species is the human race itself. Of course, this has been obvious for some time. My generation and the one before us grew up with the fear of a nuclear holocaust. Even though the number of nuclear missiles has been reduced, the list of countries possessing this technology has grown, and with it the probability that one day somebody will push the button. My children’s generation has grown up with the threat of global warming, a process whose consequences could be as destructive, albeit much slower. The human race is not very quick to understand novel threats. Just a few years ago, the president of the United States refused to ratify the Kyoto protocol on the basis that the ‘American way of life is not negotiable’, as if the core of American civilisation and values were the four-wheel drive vehicles produced by three large corporations that barely survived the end of this president’s term in office.
In this context, the one new message that the HIV epidemic, as chronicled in this book, should bring home is that well-intentioned human interventions can have unpredictable and disastrous microbiologic consequences. Mankind has emerged through a process of natural selection over billions of years. Apart from ourselves, there is probably no other living organism on earth that could destroy us completely, because if such organisms had existed, we would not have managed to reach our current status in the first place. But as I write these lines, there is renewed interest in sending humans on a wonderful voyage to Mars and back. The kids who watched Neil Armstrong’s small steps on the moon are now engineers, pilots, administrators and politicians. They think that their own generation also needs to push back a new frontier, that this is part of the human experience, and perhaps something that
will provide an answer to perennial questions about the meaning of life. For a long time I have thought that space adventures were very unwise. What is the point of setting up a small human colony somewhere in orbit around the earth or even further away, when we are systematically destroying, day in and day out, the only planet which can sustain human life? Would it not be smarter to spend our resources and ingenuity on scientific adventures whose purpose would be to protect our earth rather than taking the risk of importing into our cherished planet a completely different form of microscopic life, perhaps not even based on DNA, and whose innocuous nature has not been proven by billions of years of natural selection and co-evolution with us?

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