PIP: To determine when antibody to lymphadenopathy-associated virus (LAV) emerged in the US hemophiliac population, serum bank samples that had been collected from hemophiliacs from California, Georgia, New York, and Texas in 1968 and in 1978-84 were tested for antibody to viral proteins p25 and p41 of LAV. Antibody to LAV was not detected in the serum samples collected in 1968-69 from 15 patients with mild hemophilia A. Before 1980, it was present in only 1 of 21 California patients with hemophilia A. Among the latter group, seroconversion tended not to occur until 1982, rapidly increased in 1983, and had reached a rate of over 85% by 1984. Among Georgian hemophiliacs, 8 of 14 (57%) were seropositive in 1981 and 8 of 8 (100%) were positive in 1984. The extent of seroconversion was not as great among patients with hemophilia B as among those with hemophilia A. None of the patients with antibody to LAV has contracted acquired immunodeficiency syndrome (AIDS). Of the 22 patients who received factor VIII concentrates (21 with hemophilia A and 1 with von Willebrand's disease), 7(32%) have mild lymphadenopathy. Of the 7 patients who received factor IX concentrates (6 with hemophilia B and 1 with a factor VII deficiency), only 1 had lymphadenopathy. These findings show that LAV exposure is widespread among patients receiving factor VIII concentrate and suggest that the concentrate may have contained LAV during 1980-83. Of interest was the observation that seroconversion in hemophiliacs began shortly after the outbreak of the AIDS epidemic among homosexual men and intravenous drug users (1979-80), and the timing of seroconversion correlates with the 1st cases of AIDS in hemophiliacs in late 1981-early 1982. The temporal relationship between seroconversion and the epidemic among hemophiliacs supports the hypothesis that LAV is the etiologic agent of AIDS.