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 extraordinary — and 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 blood — a mere droplet — can 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 weeks — sometimes not for a few months — and 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.