It might seem churlish to complain about the consequences of aging with HIV

It might seem churlish to complain about the consequences of aging with HIV, when, for the first six years of the plague, survival itself was at stake. Back then, life expectancy after a first doctor’s visit was eighteen months. Tears of relief greeted AZT, a toxic old cancer drug that was reintroduced as an AIDS treatment in 1987. Researchers hoped AZT would neutralize the virus before it had a chance to cause infection. But even at doses so toxic that the drug destroyed livers and caused severe muscle loss, it proved no match for the virus’s ability to mutate. For almost fifteen years, no real hope crossed the horizon until researchers identified a promising new class of drugs. Called protease inhibitors, the pills attack cells that HIV has already infected, blocking the enzyme they use to replicate. In studies, the drugs still proved vulnerable to mutations. However, when taken in combination with the older drugs (including AZT), that vulnerability seemed to nearly vanish. What’s more, the drug cocktails somehow magnified the power of each individual drug to the point where together they could push the level of circulating virus down below the ability of sensitive tests to detect. Even more thrilling, it became clear that with the virus suppressed, the body could actually reconstitute its immune system. In most patients on successful therapy (especially those who didn’t delay or interrupt treatment), T-cell counts return to near-normal levels. Practically overnight, the number of people who developed opportunistic infections like pneumonia and Kaposi’s sarcoma dropped 70 percent.

What wasn’t clear at the time was how long patients would be expected to take these drugs. Initially, Dr. David Ho of the Aaron Diamond AIDS Research Center predicted it would be just a few years—he famously speculated that the drugs might eventually clear HIV from the system. This proved to be fantasy. We now know that HIV finds hiding places in the body out of the drugs’ reach. Once medication is halted, these sleeper cells send out armies of new viral invaders to resume the war undaunted. So the current thinking is that the drug regimens are lifelong commitments.

As a consequence, researchers fiercely debate at what point in a patient’s illness to begin prescribing them. The initial theory was an approach called “Hit early, hit hard,” meaning everyone with HIV should be on full-dose combination therapy, even those without symptoms. Alarmed by the toxic exposure, some experts began arguing to hit a little later. Federal standards were adopted that recommended the drugs to people with CD4+ T-cells under 500, a near-normal count, then were revised to 350, then 200.