The disease was known at first as Gay Related Immune Deficiency, gay cancer or gay pneumonia. Within days of the first reports appearing in Morbidity and Mortality Weekly Report (MMWR), doctors from across the USA reported similar cases.

In 1981 cases of the inexplicable immune disorder appeared in injecting drug users in New York, but it was not until the summer of 1982 that the disorder was named the Acquired Immune Deficiency Syndrome. By this time cases had also been reported amongst Haitians living in the United States and amongst hæmophiliacs, but it was not until November 1983 that the first case of AIDS was reported in a recipient of an infected blood transfusion. All of these factors, and the first report of AIDS in a woman in August 1981, lent weight to a growing medical consensus that AIDS must be caused by a transmissible agent which could be passed on in blood and through sexual contact.

Pathology logs from 18 major US cities were analysed. These suggested that AIDS cases were not spread evenly throughout the USA, but rather were confined to the major centres of New York, Los Angeles, San Francisco and Atlanta.

A typical GRID patient was a gay man in his thirties, who frequented bars and saunas, and who used poppers as a sexual stimulant. 

One of the first factors to be investigated as a cause was the use of poppers, or nitrite inhalants. Researchers found no link, but did notice that many of the earliest cases were linked: they had been one another's sexual partners. At this time researchers were working on the assumption that the disease had an incubation period of one year to eighteen months. With the benefit of hindsight, it is now reasonable to argue that this discovery was a case of drawing the correct conclusion from the wrong clues. Many of these early cases were unlikely to have been sources of infection for other cases in the early clusters; their linkage simply reflected the high turnover of partners amongst these men, and the very high level of seroprevalence of HIV in some sexual networks of gay men by 1981.

After the dismissal of poppers as a potential cause, opinion was divided between researchers on whether AIDS was caused by a single transmissible agent, in the same way as hepatitis B, or by a combination of immune suppressive factors. The latter theory, the immune overload theory, was developed as a result of the observation that all those who developed AIDS had immunosuppressive risks which might lead to the dramatic suppression of cell-mediated immunity seen in AIDS. In gay men, it was argued that repeated sexually transmitted infections combined with the use of antibiotics and the introduction of sperm into the rectum suppressed immunity. In hæmophiliacs, the repeated administration of blood products was blamed for suppressing immunity, whilst opiates and blood-borne infections were blamed for AIDS in injecting drug users. No explanation could be offered within this framework for the earliest cases of AIDS in women, except to insist that they must have been injecting drug users.

Subsequent research has shown that these factors alone cannot account for the immune suppression seen in the groups at risk of AIDS. For instance, gay men who report a high level of receptive anal intercourse but who remain uninfected with HIV do not develop AIDS. Hæmophiliacs who received Factor VIII not infected with HIV have not developed AIDS, although some studies have shown that Factor VIII is associated with a degree of immune suppression. Injecting drug users not infected with HIV do not develop AIDS either.

The search for a transmissible cause quickly became focused on the search for a retrovirus. Just months after the first cases of AIDS had been reported, virologists had already noted a similarity between the syndrome and the symptoms caused by feline leukemia virus, a retrovirus which affects cats. Research into viral causes for cancer was already well developed in the United States, and researchers in this field were quick to recognise that the hunt for an AIDS virus provided an exciting new area of research which could shed light on many of the problems they had been wrestling with for years.

HTLV-1 was the first cancer-causing retrovirus to have been identified, by Robert Gallo in 1980. His research team began looking for a virus in the same family. Meanwhile in Paris, researchers at the Pasteur Institute isolated a retrovirus from the lymph node of a gay man with early symptoms. Rather than causing lymphocytes (white blood cells) to divide, as the human leukemia virus (HTLV-1) did, this virus caused the cells to disappear. Luc Montagnier and colleagues called it lymphadenopathy associated virus (LAV). By mid-1983 Montagnier had isolated LAV from a gay man, a haemophilic and a Haitian with AIDS, but in April 1984 the US Department of Health announced that the cause of AIDS had been discovered by Robert Gallo, in the shape of a virus named HTLV-3.

Gallo was subsequently accused of stealing Montagnier's discovery, sent as a sample to Gallo's laboratory, but Gallo claimed that LAV was a different virus. LAV and HTLV-3 have subsequently been shown to be identical. The French and US governments soon entered into a patent dispute over the discovery of the virus, because financial as well as public health interests were at stake in the discovery of HIV. Testing kits were to become a major source of revenue to those who had legal rights over the virus. Huge personal prestige was also at stake. It was subsequently established that LAV was indeed the virus described as HTLV-3, and that it had accidentally contaminated Gallo's cultures.

Further reading

Mirko Grmek: The History of AIDS: Emergence and Origin of a Modern Pandemic, Princeton University Press, 1991. All the research cited in this section is referenced in Grmek's History of AIDS, the best book available on the origins of the epidemic.

Edward Hooper: The River, Penguin, 1999.

Robert Root-Bernstein: Rethinking AIDS, Free Press, 1993.