Vernon Rosario. The Gay & Lesbian Review Worldwide. Volume 20, Issue 1, Jan-Feb 2013.
The first gay person I ever met was also the first lover who died of AIDS. Tom was an ebullient bon vivant who loved to cook, built his own clavichord, and snuck me into the Episcopal church where he was the organist to play Bach works till dawn. Unbeknownst to us when we met in 1980 (my freshman year of college), HIV was silently insinuating itself into the bloodstream of men and women around the globe. It sprung into the public’s attention in 1981 after physicians published a report on an unusual outbreak of Pneumocystic pneumonia (PCP) affecting five previously healthy young gay men in Los Angeles with weakened immune systems. An editor of the Morbidity and Mortality Weekly Report noted, “The fact that these patients were all homosexuals suggests an association between some aspect of a homosexual lifestyle or disease acquired through sexual contact and [PCP] in this population.”
Soon the mysterious disease was dubbed Gay-Related Immune Deficiency, or GRID. Tom and I traveled around Europe in 1984; by then the epidemiology of AIDS and mode of transmission of HIV were better known, but it had become a terminal illness that was devastating the gay community. It was the focal point of my experience as a young gay man and gay cultural politics of the mid-1980’s. I remember attending an HIV conference at the Harvard School of Public Health, and after it was over blocking traffic on the street in front of the conference hall as part of a Boston ACT UP “die-in” to protest Reagan administration policies on AIDS drug testing and availability. No gay man or lesbian alive in the 1980’s was unscathed by the tsunami of AIDS deaths.
Tom died in 1992 while living in France, never having told anyone about his illness. His obituary in the Brown Alumni Monthly never mentioned AIDS, which was still a shameful stigma for families. I had kept all the entrance stubs from the museums and churches we had visited in Europe, planning to incorporate them into a painting inspired by a black-and-white postcard he had sent me (his last) from Grenoble, where he had died. The postcard was a close-up of sea spume fading into a black beach but could have been jism spurted out across a black canvas. I carted around the materials for the painting for a decade—to the West Coast and back East—unable to get started on the work. It was only in 1999, after a rotation in the HIV clinic at UCLA (where those first cases had been detected), that I finally was able to grapple with my memories of Tom. By then AIDS had gone from a death sentence to a treatable chronic disease thanks to an ever growing armamentarium of antiretroviral (ARV) drugs. People were living and could contemplate normal lives, albeit with expensive, complex medication regimens that had worrisome side effects of their own.
It had already become clear to me in 1986, from a molecular immunology seminar at MIT, that HIV—because of its extraordinary mutability and resilience—was also teaching us an enormous amount about the immune system at a time of exponential advances in molecular biology technology. It’s terrifying to think what the impact of AIDS would have been had the global epidemic hit a decade earlier.
It took me months to be able to open up the two books under review here, I was so resistant to revisiting the trauma of that first decade of AIDS. But the epidemiological history of 1-fly/AIDS, while tragically gripping, has a somewhat optimistic arc. The 19th International AIDS Conference in Washington, D.C., this summer buzzed with optimistic talk of the end of the disease and the goal of an “AIDS-free generation,” thanks to the latest generation of ARV drugs. Getting to this point has taken a seemingly eternal three decades in the U.S.; however, the two books under review examine its far longer history and its global impact.
The simian origins of HIV and its spread through human populations from central Africa to the rest of the world is fascinating and thoroughly interwoven with the history of African colonialism and post-independence political conflicts in each nation. Jacques Pepin covers this origins story in the dispassionate, scientific tone of the epidemiologist that he is. He calls into question the public health work of himself and others that may have unwittingly contributed to the spread of the virus. He also details health care policies and political machinations in Africa and beyond that led to the stealthy global dissemination of HIV. While there are many potential culprits in Pepin’s history, his goal is not to indict anyone, since HIV had been spreading silently for sixty or more years before it was first noted in the early 1980’s.
Far more sensationalist is the journalistic account of these events by Washington Post journalist Craig Timberg and medical anthropologist Daniel Halperin, titled Tinderbox: How the West Sparked the AIDS Epidemic and How the World Can Finally Overcome It. They track largely the same story, but with rifles in hand, eager to sniff out a conspiracy. Their work also has a peculiar authorial conceit in that, while nominally coauthored, it is delivered in the voice of Timberg, who speaks of Halperin’s research in the third person, lending it an enhanced appearance of objectivity, when in fact, Halperin has many axes to grind with AIDS bureaucrats.
T0 BEGIN with Pepin’s monograph: his account of tracking the animal and geographical origins of HIV makes for a fascinating scientific detective story. A similar retrovirus—labeled Simian Immunodeficiency Virus (SIV)—was identified in wild-born captive chimpanzees in 1989 using a human HIV test. (To date, over forty SIVs have been identified in Old World monkeys in which the viruses are mostly non-pathogenic and have been present for millennia.) Epidemiological and molecular biological research (involving collecting chimpanzee feces from the forest floor) have traced the geographic origin of the HIV-1 relative to a particular subspecies of chimpanzee (Pan troglodytes troglodytes) infected with a retrovirus that would be labeled SIV-cpz. Apparently chimpanzees are poor swimmers, so different subspecies are geographically contained by major rivers. Therefore, P.troglodytes is restricted to a large zone that includes parts of seven countries in central Africa, notably regions of the Republic of the Congo (formerly part of French Equatorial Africa), Gabon (also a former territory of French Equatorial Africa), Democratic Republic of the Congo (DRC, formerly Belgian Congo), and Cameroon (a German colony at the turn of the century until divided up between France and Britain after World War I). These countries gained independence in the early 1960’s, and their colonial history is integral to the dissemination of HIV.
Chimps are our closest genetic relatives, and the genetic similarity between HIV-1 and SIV-cpz led to the hypothesis that SIV somehow jumped from chimps to humans at one or several points before spreading through the human population. The consumption of “bushmeat,” including wild chimpanzees and gorillas, is still common in central Africa. In addition to its impact on the endangerment of species, the handling and consumption of bushmeat has been linked to the spread of monkeypox and the deadly Ebola virus. SIV infection in wild monkeys is widespread and (more recently) has been shown to be longstanding. Hunting apes is challenging, but probably became more feasible after the introduction of firearms after colonization. Pepin estimates that 1,350 adults might have been exposed to chimpanzee blood in central Africa in 1921. Therefore, many people probably were infected through bushmeat multiple times and became ill. If they had remained in an isolated jungle village, HIV would not have spread beyond central Africa. So why and when did the present HIV pandemic develop?
Tracing HIV infection back in time involves testing stored samples of human blood and tissue from storage sites around the world. The most productive places for searching for this viral needle in a haystack are samples from large public health studies, particularly of sexually-transmitted disease (STD) clinics. Another good lead are samples from patients who, before the 1980’s, suffered from unexplained immune deficiency and diseases that we now associate with AIDS, such as PCP. Applying the increasingly sophisticated immunological and genetic testing methods to these different samples allowed immunological detectives to identify early cases of HIV: a case in Kinshasa, Democratic Republic of Congo, 1970; a Norwegian family that died in 1976; a 1959 sample from the Belgian Congo; a 1960 sample from Kinshasa.
There are two species of HIV, HIV-1, and HIV-2. The first is highly virulent and easily transmitted and the cause of AIDS globally, while the second is less easily transmitted, has a longer latency, and is largely constrained to West Africa. HIV-1 mutates extremely quickly and is broken down into four main groups: M (main), 0 (outlier), N (non-M non-O), and P (only identified in 2009). HIV-1 group M is the cause of over ninety percent of HIV infections globally. It has multiple subtypes and recombinations of those subtypes (spawned in individuals infected with multiple HIV strains). Different subtypes predominate in different countries and even within distinct sexual pools: e.g., HIV-1 M subtype B accounts for 96 percent of infections in white homosexual Afrikaners, whereas subtype C is found in 81 percent of infected black heterosexuals in South Africa. HIV’s genetic complexity is like a fingerprint for epidemiologists in two important ways. First, the genetic diversity helps track the geographic spread of HIV and its transmission within sexual networks. Second, its rate of mutation allows researchers to estimate, based on the genetic disparity between viruses, how far back in time they had a common ancestor. The same techniques have been used to revolutionize the construction of the evolutionary trees not just for humans but for all living things. Based on these calculations using the historical samples, HIV-1 group M jumped from chimpanzees to humans as early as 1873 and no later than 1933, but most likely sometime in the early 20th century.
On the question of how HIV spread, Timberg largely blames the colonial exploitation of central Africa. Before the development of railroads and roads, the ivory and rubber trade relied on shipping and portage by humans. This entailed a massive recruitment of colonial subjects from inland areas to travel downriver, particularly to the cities of Brazzaville (capital of colonial Congo) and Kinshasa, DRC (formerly Leopoldville, capital of the Belgian Congo), where the material was shipped to Europe. The two cities lie directly across from each other on opposing sides of the Congo River. Hundreds of thousands of locals were also conscripted to work on the construction of railroads in the early 20th century connecting these two capitals to the Atlantic Ocean. The population of the two cities grew exponentially after WW II, with an excess of young men. Belgian Congo policy specifically discouraged wives, since workers were housed in labor camps. Therefore, prostitution thrived around them. Here were the makings of HIV’s diffusion and expansion among humans: the circulation of locals up and down river from areas with SIV/HIV, and sexual transmission in the cities. This explosive pattern has repeated itself subsequently beyond central Africa: exploitation of male labor, circulation along highways, and prostitution in urban centers.
Sexual transmission is, of course, not the only means of spreading HIV. Pepin also explores in detail blood-borne transmission—not through the sharing of illicit drug needles, but the medical use of syringes for medications and blood transfusions. He details a variety of colonial public health campaigns in the region targeting sexually transmitted diseases and other illnesses (such as sleeping sickness and tuberculosis). Aggressive treatment campaigns, especially in rural areas, sometimes relied on repeat use of needles that were unsterilized or inadequately sterilized due to time constraints or inadequate equipment and electricity. Here Pepin speaks from personal experience as a physician in the field. Again, there are numerous documented examples of such medical parenteral modes of expansion of HIV in a variety of other countries: Romania, Libya, the U.S., and China.
Pepin concludes his narrative with the passage of HIV from Central Africa to Haiti, then the U.S. Again, the unwitting effects of colonial policy may be to blame. The Belgian Congo invested little in higher education during colonial times. Most of the civil servants and professional class were Belgians. After the country’s violent lurch into independence in 1960 under Patrice Lumumba, eighty percent of expatriates fled the country. The ensuing vacuum of educational, technical, and medical expertise was largely filled by the United Nations and World Health Organization (WHO). Many of these were Haitian French-speaking professionals who jumped at the opportunity to escape the oppressive regime of Francois “Papa Doc” Duvalier and earn good salaries in the new DRC. Genetic research suggests one individual introduced the HIV-1 subtype B strain to Haiti. From there, Haitian immigration to the U.S., and gay (and straight) sex tourism from the U.S. to Haiti, would have introduced HIV to North America, where this was the sole subtype early in the epidemic. Its rapid expansion was probably the result of similar factors as in central Africa: high numbers of sexual partners in cities and the gay community, and parenteral transmission. In the Haitian case, this was due to unscrupulous plasma “farming” centers in Haiti that re-used needles, spreading the virus among locals and then through pooled infected plasma exported to the US. This produced three of the “four-Hs” identified as high risk groups in the early 1980’s: Haitians, homosexuals, and hemophiliacs (who rely on blood factors extracted from pooled plasma; heroin IV-drug users were the fourth “H”).
Timberg and Halperin’s Tinderbox provides an even broader geographical survey of the spread of HIV throughout the rest of Africa as well as Europe and Asia. The recurrent themes are the slow, stumbling, or outright delusional campaigns to deal with (or simply ignore) the spreading epidemic. The local factors are cultural discomfort with discussing sexual behavior, especially prostitution, multiple partners, and same-sex behavior. Similar reticence stymied prevention work in the U.S., where President Reagan notoriously never spoke about AIDS for four years. As in the U.S. with Elizabeth Taylor, it was often popular cultural figures in Africa who instigated the public conversation about AIDS. Uganda was one of the first and few African countries to curb the epidemic thanks to singer Philly Lutaaya, who publicized his own illness with a sympathetic call to “stand together and fight AIDS.” Thailand is another model of success where public health leaders openly and creatively promoted condom use among sex workers.
Among the external forces that Timberg and Halperin lambast is UNAIDS (the Joint United Nations Programme on HIV/AIDS). They criticize UNAIDS for over-focusing on condom promotion despite cost barriers and the success of local programs to reduce the number of sex partners. Some campaigns led by foreign public health workers struck a false note because of misreadings of local language and values. Timberg also keeps hammering away at UNAIDS’ failure to take seriously Halperin’s research on the association between male circumcision and reduced HIV transmission. Indeed, it was not until 2007 that UN-AIDS recommended voluntary circumcision and acknowledged that it led to an approximately sixty percent reduction of female-to-male HIV transmission. In high-prevalence contexts where condoms are too costly or not used, circumcision (under sterile conditions) is a cost-effective intervention. Timberg and Halperin also highlight UNAIDS’ gross overestimates of HIV prevalence (especially in Africa and Asia)—something the agency ultimately acknowledged in 2006 when it estimated that the rate of new HIV infections had peaked in the late 1990’s. We will probably never know if the AIDS pandemic panic actually helped reduce transmission or led to the squandering of resources and public numbness, if not hopeless resignation.
The tenor of current HIV research and treatment is certainly not that of hopelessness and despair, as I recall the first decade of the epidemic when Tom and other friends were dying all too regularly. New ARVs are better tolerated, once-daily pills, and they reduce viral load to near zero for most people. Therefore, the big discussion at the DC AIDS Conference was of treatment-as-prevention: placing newly HIV-infected people on ARV to reduce the risk of transmission in the population. This approach has been successful in sero-discordant couples. The drawbacks to universalizing it are its cost, the potential long-term side-effects, and abandonment of other HIV prevention tactics. As Timberg and Halperin point out in their concluding chapter on overcoming the epidemic, these multiple, well-supported tactics—such as condoms, circumcision, sexual partner reduction, needle exchange, and mother-child transmission prevention—all have their value, because HIV is not a single pandemic but manifold ones. While the picture may not be as bleak as it was early in the epidemic, HIV/AIDs remains a huge global challenge, but with intelligent political will we may be within sight of ending the further spread of HIV.