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Parenteral drug users have a high prevalence of infection with human immunodeficiency virus (HIV), the etiologic agent of acquired immune deficiency syndrome (AIDS). New York City has had a prolonged and extensive epidemic of HIV infection and AIDS. In this study, we analyze, in relation to antibody to HIV (anti-HIV), available data from sera from parenteral drug users collected in New York City during 1978 through 1983 in the course of studies of liver disease. Among parenteral users of both heroin and cocaine, 30 (52%) of 58 had anti-HIV, compared with six (13%) of 48 injectors of heroin only (P less than 0.0001). Only two (11%) of 18 white patients were HIV-infected, compared with 34 (39%) of 88 black or Hispanic patients (P = 0.03). No other factors studied were linked to anti-HIV. In a multiple logistic regression, anti-HIV was significantly more common in parenteral users of both cocaine and heroin (P less than 0.0001), black patients (P = 0.02), and Hispanic patients (P = 0.049). We conclude that parenteral users of both cocaine and heroin as well as black and Hispanic patients were disproportionately HIV-infected during the early years of the HIV epidemic. Use of cocaine and heroin as well as ethnicity were independently linked to anti-HIV. Measures to prevent or treat drug use, HIV infection, and other medical problems while addressing the specific needs of cocaine users and black and Hispanic patients are urgently needed.

Intravenous drug users are the second largest group to develop the acquired immunodeficiency syndrome, and they are the primary source for heterosexual and perinatal transmission in the United States and Europe. Understanding long-term trends in the spread of human immunodeficiency virus among intravenous drug users is critical to controlling the acquired immunodeficiency syndrome epidemic. Acquired immunodeficiency syndrome surveillance data and seroprevalence studies of drug treatment program entrants are used to trace seroprevalence trends among intravenous drug users in the borough of Manhattan. The virus entered this drug-using group during the mid-1970s and spread rapidly in 1979 through 1983. From 1984 through 1987, the seroprevalence rate stabilized between 55% and 60%--well below hepatitis B seroprevalence rates. This relatively constant rate is attributed to new infections, new seronegative persons beginning drug injection, seropositive persons leaving drug injection, and increasing conscious risk reduction