Sexual behavior before AIDS: the hepatitis B studies of homosexual and bisexual men.

Data on sexual practices, collected during studies of hepatitis B virus (HBV) infection in 1978 and 1979, were analyzed for 4910 homosexual and bisexual men from Chicago, Denver, Los Angeles, San Francisco, and St Louis. Data on sexual practices in 1978 showed that white participants had larger numbers of non-steady male sexual partners and engaged in oral-genital activities more frequently but were equally likely to engage in anal intercourse as black and Hispanic participants. San Francisco participants had more non-steady sex partners and were more likely to engage in receptive anal intercourse with non-steady partners than participants from all other sites. Analysis of data on 606 HBV-antibody-negative men interviewed on three occasions in 1978 and 1979 showed no changes in risk indices for insertive and receptive anal intercourse between these years, except in San Francisco where significant declines occurred in insertive anal intercourse and receptive anal intercourse without ejacultion in a small, highly select group of participants.

Sexually transmitted diseases and homosexuality.

An epidemic of sexually transmitted diseases, culminating in the emergence of acquired immune-deficiency states, has developed among homosexually active men during the past ten to 15 years. This epidemic is reviewed in relation to causative factors, priorities for control, and recommendations for control and prevention. Causative factors are divided into physical, behavioral, cultural, and political factors. Given the complicated interactions of these factors and the numerous diseases epidemic in the homosexuality active population, priorities need to be established for research and control programs that take into account the overall health impact of each disease and the effectiveness of available and potential resources. Finally, educational programs must be developed that will overcome the limited effectiveness of public health control efforts in this area, or we may expect even more serious and widespread health care problems.

Delta hepatitis in homosexual men in the United States.

To assess the incidence and prevalence of delta hepatitis in homosexual men, we tested serum specimens for delta markers in participants in two previous studies: a hepatitis B vaccine trial among homosexual men conducted in the early 1980's and the Centers for Disease Control sentinel counties hepatitis study for 1983-1984. In the vaccine trial, men found to be hepatitis B surface antigen positive at the time of enrollment and those men who had serologic evidence of new hepatitis B virus infection during follow-up were tested. In the sentinel counties study that determined risk factors for viral hepatitis in reported cases, all homosexual men with acute and chronic hepatitis B virus infections were tested for delta markers. Specimens were tested for delta antigen and IgM and total delta antibody. In seven different cities, among 321 men found to be HBsAg positive at the time of screening, eight (2%) were positive for any delta marker. Among 290 men with new hepatitis B virus infections during follow-up, three (two coinfections, one superinfection) had serologic evidence of delta hepatitis. In the sentinel counties study, 0/63 acute hepatitis B virus infections in homosexual men were associated with delta hepatitis. This study indicates that the delta agent is an infrequent cause of viral hepatitis in homosexual men in the United States.

Long-term immunogenicity and efficacy of hepatitis B vaccine in homosexual men.

To study the duration of antibody persistence and protection provided by the hepatitis B vaccine, we followed 773 homosexual men for five years after completion of vaccination. Among the 635 participants in whom antibody levels above 9.9 sample ratio units (SRU) developed after vaccination, 15 percent lost antibody altogether, and in another 27 percent, antibody levels declined below 10 SRU within five years. The extent of the maximal antibody response strongly predicted the persistence of protective antibody. Hepatitis B infection occurred in 55 men; 8 of these infections were clinically important (characterized by the presence of the hepatitis B surface antigen and elevation of liver-enzyme levels), and two of the patients became hepatitis B virus carriers. The long-term risk of hepatitis B infection was inversely related to the maximal antibody response to vaccine. Most severe infections occurred among those who responded poorly or had no response to the vaccination. The risk of late infection with hepatitis B in those with an initially adequate vaccine response increased markedly when antibody levels decreased below 10 SRU, but only 1 of 34 late infections resulted in viremia and liver inflammation. A second series of vaccinations induced a moderate antibody response in 50 percent of the subjects who initially had no response or a poor response; however, the persistence of antibody was poor. Both antibody loss and the risk of severe disease should be considered when booster-dose strategies for the hepatitis B vaccine are being designed.

Outcome of hepatitis B virus infection in homosexual men and its relation to prior human immunodeficiency virus infection.

To investigate the effect of human immunodeficiency virus type 1 (HIV-1) infection on subsequent hepatitis B virus (HBV) infection, HIV antibody was sought in homosexual men who developed HBV infection during a hepatitis B vaccine trial. Among 134 unvaccinated HIV-1-negative men, 7% became HBV carriers, 64% had viremia, and 42% had clinical illness. Among vaccinated HIV-1-negative men, HBV infection severity decreased with number of vaccine doses administered. When adjusted for prior hepatitis B vaccination status, persons with HIV-1 infection preceding HBV infection had a significantly higher risk of developing HBV carriage, viremia, prolonged ALT elevation, and clinical illness. Among HIV-1-infected men, the risk of HBV carriage was increased in unvaccinated persons (21%) and those who failed to respond to vaccination (31%) and further increased in those who received vaccine doses at the time they developed new HBV infection (56%-80%), suggesting inactivated hepatitis B vaccine may temporarily impair the immune response to HBV infection in HIV-1-infected persons. HIV-1 infection was also associated with reduced alanine aminotransferase elevations during the first 36 months of follow-up of men who became HBV carriers.