Two families of gorillas, comprising 13 animals, were studied in 1980-1982 for hepatitis virus infections. It was found that 27% of them had evidence of hepatitis B infection, and 23% evidence of hepatitis A infection. The four parents had been born in the wild and all of them had been infected with hepatitis B. The two patriarchs were positive for hepatitis B surface antigen (HBsAg) and one had hepatitis Be antigen (HBeAg). The two matriarchs had antibody to hepatitis B surface antigen. Three of the four parents had antibody to hepatitis A virus. The two gorillas with HBsAg were retested two years later and shown to be chronic carriers of HBsAg, subtype adw. Both were HBeAg positive at this time. Six of the nine children in the first generation born in captivity had antibody to hepatitis B, but none of them had antibody to hepatitis A. Two gorillas were documented by seroconversion to become infected with hepatitis B, indicating gorilla-to-gorilla transmission. During the course of this study, a recently employed keeper who had the most direct contact with the gorillas experienced an asymptomatic seroconversion to hepatitis B. This study indicates that hepatitis B in gorilla families in captivity may be a model of its behavior in human families, and that close, continuing contact with gorillas may be an occasional source of human infection.
Measles immunity was studied in children in a private pediatric practice who had been revaccinated because they had received their primary measles vaccination before 1 year of age. Antibody was measured in 72 of these children who had received the first injection of live measles virus vaccine at <10 months of age, and the second at >1 year of age. Of the 72 children, 29 (40%) had no detectable antibody and the geometric mean titer for the group was approximately 1:4. Of the children with low antibody titers, 15 were given a third injection of measles vaccine and five (33%) still did not respond. Cell- mediated immunity as indicated by lymphocyte transformation to measles antigen was measured in 11 of the children. Five (45%) had responses to measles antigen, but the responses did not correlate with the presence or absence of antibody. This study confirms the observation that revaccination is unsuccessful in many children who received measles vaccine in the first year of life, and shows that even a third injection of vaccine may fail to produce a significant antibody response.
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