Current research is targeting the ability of H.I.V. to stay dormant in memory T cells. Illustration by Harry Campbell

One morning in the winter of 1981, my wife came home after her on-call shift at the U.C.L.A. Medical Center and told me about a baffling new case. Queenie was an eighteen-year-old prostitute, his hair dyed the color of brass. He had arrived at the emergency room with a high fever and a cough, and appeared to have a routine kind of pneumonia, readily treated with antibiotics. But the medical team retrieved a microbe from his lungs called Pneumocystis carinii. The microbe was known for causing a rare fungal pneumonia that had been seen in severely malnourished children and in adults undergoing organ transplants or chemotherapy.

Several specialists at the hospital were enlisted to make sense of the infection. Queenie had a critically low platelet count, which made him susceptible to hemorrhage, and I was called in to examine him. He was lying on his side and breathing with difficulty. His sheets were soaked with sweat. A herpes infection had so severely blistered his flesh that surgeons had cut away necrotic segments of his thighs. I couldn’t explain his falling platelet numbers. His lungs began to fail, and he was placed on a ventilator. Soon afterward, Queenie died, of respiratory failure.

His was one of several cases of the same rare pneumonia seen by physicians on both coasts. Michael Gottlieb, a U.C.L.A. immunologist, studied the blood of some of these patients and made the key observation that they had lost almost all their helper T cells, which protect against infections and cancers. In June, 1981, the Centers for Disease Control published Gottlieb’s cases in its Morbidity and Mortality Weekly Report, and, in July, Dr. Alvin Friedman-Kien, of New York University, reported that twenty-six gay men in New York and California had received diagnoses of Kaposi sarcoma, a cancer of the lymphatic channels and blood vessels. This, too, was strange: Kaposi sarcoma typically affected elderly men of Eastern European Jewish and Mediterranean ancestry.

I tended to our Kaposi-sarcoma patients. I was the most junior person on staff and had no expertise in the tumor, but none of the senior faculty wanted the job. My first patient, a middle-aged fireman nicknamed Bud, lived a closeted life in West Los Angeles. Not long before he checked in to the hospital, he had started to find growths on his legs that looked like ripe cherries. Then they appeared on his torso, on his face, and in his mouth. Despite strong doses of chemotherapy, the standard treatment for advanced Kaposi sarcoma, his tumors grew, disfiguring him and killing him in less than a year. By 1982, men with highly aggressive kinds of lymphoma had started to arrive at the hospital. They, too, failed to improve with chemotherapy. Patients were dying from an array of diseases that had overcome ravaged immune systems. All my patients had one disorder in common, which the C.D.C., that year, had named acquired-immunodeficiency syndrome, or AIDS. Scientists did not yet know what caused it.

The next year, two research teams—one led by Luc Montagnier and Françoise Barré-Sinoussi, of the Pasteur Institute, in Paris, the other by Robert Gallo, at the National Cancer Institute, in Maryland—published papers in Science that described a new retrovirus in the lymph nodes and blood cells of AIDS patients. A retrovirus has a pernicious way of reproducing: it permanently inserts a DNA copy of its genome into the nucleus of a host cell, hijacking the cell’s machinery for its own purposes. When the retrovirus mutates, which it often does, its spawn becomes difficult for the body or a vaccine to target and chase out. Retroviral diseases were widely believed to be incurable. In May of 1986, after much dispute about credit for the discovery (the French finally won the Nobel, in 2008), an international committee of scientists agreed on the name H.I.V., or human immunodeficiency virus. By the end of that year, about twenty-five thousand of the nearly twenty-nine thousand Americans with reported AIDS diagnoses had died.

Since then, H.I.V. has been transformed into a treatable condition, one of the great victories of modern medicine. In 1987, the F.D.A. approved AZT, a cancer drug that had never gone to market, for use in H.I.V. patients. At first, it was extortionately priced and was prescribed in high doses, which proved toxic, provoking protest from the gay community. But AZT was able to insinuate itself into the virus’s DNA as it formed, and later it was used in lower doses. Scientists have now developed more than thirty antiretroviral medicines that stop H.I.V. from reproducing in helper T cells.

The idea of combining medications into a “cocktail” came in the mid-nineteen-nineties, mirroring the way oncologists treated cancer. Cancer cells, like H.I.V. particles, can mutate quickly enough to escape a single targeted drug. The treatment regimen—HAART, for highly active antiretroviral therapy—was put through clinical trials by prominent researchers such as David Ho, of the Aaron Diamond Institute, in New York. I gave the cocktail to one of my patients, David Sanford, and less than a month after beginning treatment his fever fell, his infections disappeared, his energy returned, and he started to gain weight. The H.I.V. in his bloodstream plummeted to an undetectable level, where it has remained. Later, in a Pulitzer Prize-winning article, Sanford wrote, “I am probably more likely to be hit by a truck than to die of AIDS.” That now holds true for a great majority of people with H.I.V. in the United States. In the past five years, not one of the dozens of H.I.V. patients I’ve cared for has died of the disease.

There are still tremendous hurdles. Thirty-five million people in the world are living with the virus. In sub-Saharan Africa, where most new cases are reported, sixty-three per cent of those eligible for the drug regimen do not receive it; those who do often fail to receive it in full. In the United States, a year’s worth of HAART costs many thousands of dollars per patient, and the long-term side effects can be debilitating.

Now researchers are talking more and more about a cure. We know as much about H.I.V. as we do about certain cancers: its genes have been sequenced, its method of infiltrating host cells deciphered, its proteins mapped in three dimensions. A critical discovery was made in 1997: the virus can lie dormant in long-lived cells, untouched by the current drugs. If we can safely and affordably eliminate the viral reservoir, we will finally have defeated H.I.V.

Ward 86, the nation’s first outpatient AIDS clinic, opened at San Francisco General Hospital on January 1, 1983. Recently, I went there to see Steven Deeks, an expert on the chronic immune activation and inflammation brought on by H.I.V. Deeks, a professor at the School of Medicine at U.C.S.F., also runs the SCOPE Study: a cohort of two thousand H.I.V.-positive men and women in whom he measures the long-term effects of living with the virus. Each year, blood samples are sent to labs all over the world. Deeks’s mission is to catalogue the damage that H.I.V. does to tissues and to test new drugs that might help.