No Time to Lose: A Life in Pursuit of Deadly Viruses (19 page)

By this time, the European Union had set up a Task Force on AIDS, and was beginning to send money to fund AIDS-related projects, as a form of emergency development aid. Lieve Fransen, the Flemish doctor who had worked in our research project in Kenya and then moved to Antwerp to earn her PhD, was running this task force. One day she called me and asked whether I was interested in developing an AIDS control program in Lubumbashi, the capital of Shaba province in southeastern Zaire.

This project wasn’t about doing research. It was about doing what needed to be done: provide a safe blood supply, try to improve the public health service in general by training people, and rehabilitate the medical lab so they could properly diagnose. It was the work of a nongovernmental organization, and I was an academic. Nonetheless, when I thought it over I found that I wanted to do it. I wanted to do something practical about AIDS, with direct impact on public health. Instead of studying reality, I wanted to actually change it.

The first thing we did once the project actually got started, in 1988, was to refurbish the public health laboratory, which meant new equipment and an architect—even the roof had to be rebuilt. I became like a manager of a big operation, though Drs. Kambali Magazani from Zaire and Geert Laleman from Antwerp ran the project on-site. All kinds of things went wrong, from using rapid tests for blood that were sensitive to fluctuations in temperature and had a short shelf-life to incorrect readings. Things broke and shifted and rotted. I quickly learned that funding was not the only hurdle to an organized project, and not just in Africa but everywhere.

I remember a midwife at the hospital. She had AIDS: fungal and herpetic infections in the mouth, intractable diarrhea. There was a Tanzanian pathologist and he told me that in 15 years he had never seen anything like the swollen lymph nodes he was now seeing daily. There clearly was AIDS in Lubumbashi, and I felt I was watching the epidemic move in, but it was doing so in slow motion. HIV prevalence was low—something like 3 percent, compared to the 6 percent we estimated in Kinshasa—and the incidence, the measure of
new
infections, didn’t seem to be explosive. The big question was, Would it stay this way?

We were 1000 miles away from Kinshasa, deep in southern Africa. The Shaba province (and Lubumbashi) is a kind of panhandle that sticks way down south into Zambia in an awkward, artificial-looking shape. And yet, in the Zambian copper belt, just across the border, the prevalence of HIV was far higher—over 15 percent—and it was spreading much more quickly.

Since colonial times the miners were permitted to live in Lubumbashi alongside their families. The Belgian mining companies built family housing and schools, they hired the sons of miners. It was a different setup from the system that mining companies created in Zambia, with tens of thousands of single men away from their families, living in hostels, doing a terrifying dangerous job, with recourse to prostitution often their sole sexual expression. Was this the explanation for the difference in HIV levels? We still do not know. Again I realized that there was not going to be one AIDS epidemic in the world but many different ones, depending on behavior and culture, and that any kind of solutions that could be put together were going to have to be tailor-made.

IN 1988 MANN
organized a major ministerial conference in London that was attended by 115 ministers of health, more than had ever gathered on a specific disease. Before that meeting, Minister Ruhakana Rogunda from Uganda was the lone voice who in a dramatic speech at the World Health Assembly in 1987 had called his peers to face the reality of AIDS on their continent. Even though many attending the London meeting were still in denial about the scale of the problem in their own countries—and several came from governments that had pledged to shut out foreigners with HIV—all of the ministers signed off on a declaration backing the human rights and dignity of people living with HIV. This had not been a foregone conclusion by any means. Since Mann’s arrival in 1986, WHO had been giving governments a range of services, from technical help with drawing up three- to five-year AIDS plans, to funds for new laboratories and training programs for medical professionals; it was even fund-raising from Western governments to support AIDS programs in poor countries.

The budget for the Global Programme on AIDS had grown bigger than any other single program at WHO, but it was raised directly from donor countries: it didn’t come from WHO’s general budget. The name itself, Global Programme on AIDS (GPA), emphasized that this was not a temporary or short-term emergency. Jonathan Mann also established a Global Commission on AIDS with highly respected political and scientific figures, to protect him, I think, from the political pressures.

Halfdan Mahler’s term of office as director-general of WHO came to an end. He had received multiple complaints about Jonathan from irate ministers of health who felt pressured to address AIDS but the two of them had developed a good working relationship, with a lot of mutual respect. Hiroshi Nakajima, formerly the WHO regional director for Asia, was appointed as the new director-general. This was a whole different story.

Mann had done something very unusual for WHO since the eradication of smallpox. He directed his short-term plans straight out of headquarters: he completely bypassed the regional offices and sent his staff and temporary consultants to each country. This really was the only solution, otherwise in many countries there would have been virtually no movement to ward off the epidemic. But in doing this he created powerful resistance against him from the regional directors who control around three-quarters of the WHO budget.

Jonathan had the guts and political acumen to convene a meeting of the Global Commission on AIDS in Brazzaville—the city that hosted WHO’s regional office for Africa—in essence forcing the regional director to confront the reality of AIDS in Africa under the impatient eyes of eminent persons from across the world. This is when I met one of Asia’s marketing geniuses, Senator Khun Meechai Viraidya from Thailand, who was a member of the commission. We got to know each other when I was looking for someone of my height to ask to lend me fresh clothes, as my suitcase had not arrived (and neither had Jim Curran’s). Meechai immediately gave me a suitcase full of all I needed, and we became friends for life. Meechai was a businessman, politician, and community leader—an entrepreneur in many respects, and above all a superb communicator. He became the architect of Thailand’s successful AIDS program, imposing 100 percent condom use in commercial sex, which was flourishing in Thailand. This ultimately led to a decline of HIV in the country—one of the very early achievements in HIV prevention in the world.

In the meantime HIV continued its spread over the world, discriminating nowhere. The Soviet Union reported its first case in 1987, and in November 1988 I went to Moscow with a team of Belgian AIDS experts to share our experience with our Russian colleagues, who were very concerned about further spread of HIV in their vast country. Until then all AIDS patients from the USSR had been hospitalized, often for months, in the Institute for Infectious Diseases in Moscow. While Dr. Vadim Pokrovsky, the top soviet AIDS epidemiologist, was showing us around in his institute I suddenly saw three Africans at the end of the corridor. I tried my luck and shouted, “Bonjour!” The three men rushed to me, happy to be able to tell their sad story in a language they mastered far better than Russian. They were students at Lumumba University from Burkina Fasso and Burundi, had tested positive for HIV on arrival in Russia, and had spent several months in what was basically quarantine, even if they were in good health. I promised I would bring up their case with the authorities to see if they could help these students. Just like small Belgium, the Soviet Union was confronted with multiple entry points for HIV. Little did we know at the time that Russia and the former Soviet republics would experience a still-growing HIV epidemic driven by injection drug use.

It was my first visit to Moscow, and I don’t pretend I fully understood what was going on, particularly in the quite secretive days of the Soviet Union. But there was clearly change in the air among health colleagues, who were eager to connect with us. It was already bitter cold, but the people were warm once we socialized.

IN ANTWERP, OUR
lab started using simple techniques to look at pieces of the genome of all kinds of isolates of HIV-1. At some point these strains had been grouped into A, B, C, D, and so on, based on the sequences of the envelope gene, and there was a great deal of discussion of their relative pathogenicity and how you could develop a vaccine to protect against them all—a still-unresolved challenge. When in 1989 members of my team, Bob De Leys and Martine Peeters, isolated two very unusual HIV-1 strains from a couple from Cameroon, the genetic variation of HIV appeared to be even wider than we thought. The woman was nineteen and both she and her husband had persistent generalized lymphadenopathy, but their serum gave only faint bands in the confirmatory Western blot test. The virus that we found in it was very aberrant. (We called it ANT70, though it is now known as Group O: Group “Oh” not Group “Zero.”) It had major differences with all the known strains of both HIV-2 and HIV-1, and was particularly divergent in the envelope glycoprotein. Sampling indicated that 5 to 8 percent of HIV-1 infected individuals in Cameroon harbored the Group O variant, but five additional strains of HIV-1 subtypes (A, B, E, F, and H) were also found. It seemed that in Cameroon and surrounding countries such as Gabon, the greatest diversity of HIV strains were circulating, suggesting that the virus had had more time to diversify there than elsewhere.

This was not good news. Already we were dealing with HIV-1 and HIV-2: two viruses that created the same pathology but that were genetically quite distinct. We already knew that people could be infected with both different families of HIV viruses at the same time. If, in addition, strains within each of these families diverged to this degree, we were in trouble; it would tremendously complicate the development of a vaccine against HIV infection.

Per molecular clock calculations, Group O seemed to be the oldest virus strain yet identified. It may be even older than SIVcpz, a virus closely related to HIV-1 that Belgian microbiologist Martine Peeters had also found in a pet chimpanzee named Amandine in Gabon. (SIV denotes a
simian,
or monkey, virus and cpz is for chimpanzee.) That discovery came more or less by chance, when Martine and her French husband, Eric Delaporte, were screening monkeys and apes for HTLV human T-lymphotropic virus (a virus that can cause T-cell leukemia and myelopathy/tropical spastic paraparesis in humans). They were working in Franceville at a medical research center funded by the French petroleum company ELF-Aquitaine, and we maintained close contact with them from Antwerp (they sent us samples of gonococcal stains). All of us were stunned when an apparently healthy chimpanzee was found to have a virus almost identical to human HIV. In fact the chimpanzee virus so closely resembled HIV-1 that initially Martine’s publication was refused: there was disbelief that this was possible; the viruses were so similar that reviewers assumed it must be due to a lab contaminant. When Martine was back in Antwerp working in our team, she found a second SIVcpz in a chimpamzee named Noah, living in the zoo in Antwerp. He was healthy as was Amandine and is now living in a chimpanzee hotel in the Netherlands.

Many viruses have species-jumped at some point, and these are the viruses that overwhelm their new target group with epidemics, because no immunity has yet developed against them. So this research contributed to exploring the complexity and diversity of HIV, and to showing that its greatest diversity is in west Central Africa, specifically Cameroon and Gabon. I don’t like the term “Ground Zero,” which suggests a single, explosive event: the transition from ape virus to human virus was more like a kind of seepage. But this place is probably where it first happened.

In addition we found an extremely rapid rate of gene mutation, faster even than the flu virus. We did a lot of work on characterizing virus isolates, and following particular strains as they grew in various populations. For example, in Thailand there seemed to be several, fairly separate HIV epidemics under way, in gay men, heterosexual prostitutes, and injection drug users.

Could we find any kind of antibodies that would neutralize every possible strain of HIV? Some antigen, some piece of envelope protein, that could be a clue to help develop a vaccine? We began working on it in the late 1980s. It was painstaking work—monks’ work. And it came up with no practical results. (It was not until 2010 that researchers found any such antibodies.) The reality is that a lot of scientific research goes nowhere. Medical researchers have a saying: if you want quick results, become a surgeon.

In other areas at least, we were getting results. Studies in Rwanda by Philippe Vandeperre, and in Nairobi by Pratibha Datta, Joan Kreiss, and Joanne Embree, told us that children who were breast fed by HIV-positive mothers had a higher rate of infection than children who were not, particularly for women who were newly infected during their pregnancy. This confirmed our suspicion that recent infection led to a high viremia and far higher probability of transmission, but it also indicated that HIV was transmitted through breast milk more often than we had previously thought.

Frank Plummer in Nairobi made another fascinating observation. Some of the prostitutes who had been attending our clinic in Nairobi for years—women who were well known to us, who had literally had thousands of sex partners, and indeed several bouts of sexually transmitted disease—did
not
become infected with HIV. It was almost a Sherlock Holmes–type of observation—the dog that
didn’t
bark—but once he started thinking about it, it popped up again and again.

We came up with about two dozen women who appeared to be immune to HIV. Despite counseling, they didn’t always use condoms. But either their immune system was better equipped to recognize HIV-infected cells and remove them, or they had fewer target cells for HIV to infect in the first place. The good news was, the women’s constant exposure to the HIV virus reinforced their ability to fight the infection. The bad news was, if their exposure was stopped, even for a matter of weeks—if they took a break from sex work and returned to their villages—they lost their immunity. Frank and his team are still working on this immunological exception, and one day it may bring a clue to the development of a vaccine.