I first became interested in HIV and AIDS in the late 1980s, when the ‘Don’t Die of Ignorance’ campaign was running on British TV screens.
So little was known about the virus, and how it worked, that prominent virologists argued over whether HIV even caused AIDS. For a while, the ‘dissenters’, as they unfortunately came to be known, raised interesting questions. Why was the latency from infection to disease so long? Why did the virus cause so many disparate diseases? Why was it so hard to isolate the HIV virus from a patient with full-blown AIDS? And so on.
Gradually, those questions were answered. HIV hijacks the immune system and sets it against itself in a war of attrition. Some patients are able to fend the virus off for longer, but it is a losing battle, and eventually the immune system falters. In the end, the immune system can do little but fend off the replicating HIV, leaving the patient vulnerable to a host of opportunistic infections. This is why HIV sufferers can develop a large number of other diseases, while, paradoxically, expressing little of the virus itself – their immune system is still wiping it out.
When they were uncovered, these facts about HIV were depressing. Nobody knew how to prevent a virus that did what HIV did. A vaccine seemed unlikely, a cure impossible. The potential spread of the virus was exaggerated for political gain, but there was a central reality: HIV infection pointed only towards severe illness and premature death.
Then the impossible started to happen. Antiretroviral drugs were developed that held the virus in check, and, when taken continuously, slowed or prevented premature death. The drugs also attenuated transmission of the virus through pregnancy and sexual contact. As the drugs have improved, so the virus has retreated further and further. However, patients with HIV still have to keep taking antiretrovirals, because the virus recedes and lies dormant. Once the patient stops taking the drugs, it re-emerges.