Real breakthroughs in AIDS research have been painfully few, but at least 1995 saw a handful of provocative research reports. The biggest came in January, when two groups found that the AIDS virus reproduces--and is cleared from the body--at much higher rates than previously suspected. It had been thought that HIV turns virulent only in the late stages of infection, but apparently the virus works its devastation through rapid and prolonged replication. Over the course of a decade-long infection, millions of viral variants are spawned, ultimately infecting immune cells faster than the body can replace them.
But if the immune system is strong enough to keep pace with the virus throughout the first years of infection, why can’t it do so permanently? Apparently it can--if it’s given enough warning. A report published in June showed that infection with a milder strain of the virus-- called HIV-2--sometimes protects people against infection with the more virulent HIV-1. HIV-2, in other words, seems to work like an AIDS vaccine.
In the long run HIV-2 can still cause AIDS. But it is so comparatively mild that people rarely develop symptoms after even a decade of infection, says Max Essex, a Harvard virologist and coauthor of the study. Although the two strains bind to the same receptor on immune cells, HIV-2 doesn’t bind as tightly, making it harder for the virus to work its way into the cell and replicate. While HIV-1, which originated in central Africa, now infects some 20 million people worldwide, HIV-2 is rare outside West Africa, where it infects a few million people--and where, significantly, it is more common than HIV-1.
HIV-2 was in West Africa long before HIV-1, says Essex, so we could ask the question, if people are already infected with HIV-2, did they experience lower rates of subsequent infection with HIV-1? He and his colleagues conducted a nine-year study of 700 female prostitutes in Dakar, Senegal, and found that women already infected with HIV-2 were three times less likely than virus-free women to become infected with HIV-1.
Presumably, infection with HIV-2 revs up the immune system, alerting T cells to look out for proteins shared by the two strains. Once researchers have identified the proteins that stimulate the immune response, says Essex, they may be able to insert the appropriate genes into a harmless virus to create a safe live vaccine.
Another provocative study, reported last January, hinted that some kinds of natural exposure to HIV may prime the immune system as effectively as a vaccine. British researchers studied six female prostitutes in Gambia, West Africa, five of whom, although repeatedly exposed to both HIV-1 and HIV-2, showed no signs of infection--no virus, no HIV antibodies. Yet when T cells--the immune cells that detect viruses-- were taken from some of the women and exposed to cells bearing key HIV proteins, the T cells killed the cells, a clear sign that the women’s immune systems had squared off with the virus before.
Andrew McMichael, one of the study’s authors, suspects that these women may have been infected with HIV so weak or in such low dosage that the infection was swiftly eliminated before it could take hold. The implication is that perhaps these women have been infected and cleared the infection, says McMichael. Since they’ve already been exposed, this immune response might be protecting them from further infections.
