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But the virus leaves other traces. The immune system has two main arms: antibodies, which attack viruses floating free in the bloodstream, and cytotoxic T-lymphocytesor killer T-cellswhich destroy the body's own cells that have been infected. Like antibodies, killer T-cells are specific to one microbe, so they, too, are a kind of fingerprint.
What happens is that an infected cell displays on its outer membrane fragments of the virus called epitopes. Killer T-cells that recognize these particular epitopes destroy the infected cell. What's more, the immune system clones millions of killer T-cells that are specific to those epitopes, in order to wipe out all the cells the virus has infected. So, high numbers of HIV-specific T-cells indicate that the virus was present.
Oxford researcher Andrew McMichael is one of the world's leading experts on the killer T-cell. McMichael and his colleague Sarah Rowland-Jones had studied multiply exposed yet uninfected sex workers in the West African nation of the Gambia, and many of them had elevated numbers of HIV-specific killer T-cells. But in the world of the multiply exposed, the Gambian sex workers couldn't hold a candle to the Pumwani prostitutes. They were the acid test.
Plummer's team had found evidence of HIV-specific killer T-cells, but many scientists weren't convinced. Collaborating with Plummer, the Oxford researchers verified the findings, banishing virtually all scientific doubt: The women really had been exposed to HIV, and their bodies had mounted a defense with killer T-cells.
Could those cells be the key to protection?
As scientists learned more about HIV's initial assault on the body, it became clear that the immune system always mounts a vigorous counterattack. In fact, what happens in the first few weeks after infection is nothing short of extraordinaryand it bolsters the current consensus that killer T-cells are critical to warding off HIV.
What typically happens is this: The surfaces of certain cells in the body are studded with two molecules, named CD4 and CCR5. If the virus chances upon such a cell and binds to these molecules, then, like a burglar picking a lock, HIV gains entry, commandeers the cell's DNA, and forces it to churn out as many as 10,000 new viruses. These are ejected from the cell to float in the body, waiting to enter new cells.
Within 48 hours, swarms of viruses have advanced from the site of infection into the lymph nodes, where HIV's favorite immune-system cells abound. In as little as three days, the virus has infiltrated certain long-lived cells where it can hide out during years of ferocious medical assault and still emerge to rekindle the infection. By the 10th day, HIV has usually spread to the brain, spleen, and gut. At this point in the invasion, the amount of HIV in the blood soars to almost unbelievable levels: A single milliliter of blooda mere dropletcan be teeming with as many as 95 million viruses.
Then the immune system rallies. The body produces millions of HIV-specific killer T-cells that attack infected cells and also excrete special molecules that can paralyze HIV. Antibodies against the virus won't appear in the blood for about two more weekssometimes not for a few monthsand they seem to have little effect. It is the killer T-cells that appear to suppress the virus.
Yet they don't eliminate it. Instead, the virus and the immune system become locked in a pitched battle that lasts for years. Eventually, for reasons that are still not understood, HIV overwhelms the immune system, rendering the patient vulnerable to whatever diseases come along.
Those initial days of infection, when the body becomes saturated with virus, are the key to a vaccine, McMichael believes. Killer T-cells are "always chasing the virus," he says, "and the virus is always one step ahead. But if a person is vaccinated, then the immune system starts out ahead."
So what McMichael and his team have done is construct a vaccine made from the DNA of epitopes that killer T-cells recognize. He's made sure that these virus fragments come from parts of HIV that don't mutate and so can't change to escape the T-cells' attack. Some of the epitopes in the vaccine are ones targeted by killer T-cells of the exposed but uninfected Pumwani prostitutes. "The vaccine," says Plummer, "was built in part around these women."
After safety trials in England starting early next year, the vaccine will go into trials in Nairobi. Maybe a vaccinated immune system can eliminate the virus before it gains a foothold. Or, barring that, maybe the vaccine could help the body suppress the virus to such low levels that it would be hard to transmit and never cause disease.
Selina, not her real name, blocks out the difficult parts of her life. She claims, for example, that she cannot recall the first time she had sex for money. But she revels in the scraps of good fortune that come her way, such as the fact that she never got HIV. Like Joyce, she had been in Plummer's original 1985 cohort, and like Joyce she didn't get infected. She bragged that she was immune. But today, when asked if she used to think she was invulnerable to the virus, she answers in a non sequitur, saying that she has to be careful because some men remove their condoms "in a tricky way."