Sera from 113 multiply transfused patients with bleeding disorders of whom 92 (81.4 per cent) were hemophiliacs were tested for such hepatitis‐B virus (HBV) markers as HBsAg, anti‐HBs. anti‐HBc, e‐antigen and anti‐e. For comparison these marker tests were conducted on sera from 398 apparently healthy blood donors, 198 were previously known to be both HBsAg and anti‐HBs negative, 126 were anti‐HBs positive and 74 were HBsAg positive. Among patients with bleeding disorders, overt HBV infections were infrequent (2 per cent) and there was a low prevalence of HBsAg (3.5 per cent), e‐antigen (1 per cent) and anti‐e (0 per cent). However, the prevalence of anti‐HBs (63 per cent) and anti‐HBc (55 per cent) was high. Of the 71 anti‐HBs positive patients with bleeding disorders 54 (76 per cent) were also anti‐HBc positive. The sera of only four patients contained anti‐HBc alone. All but one of the patients with bleeding disorders who were anti‐HBc positive exhibited persistent responses. Anti‐HBc was detected in all the HBsAg positive blood donors and in 113 of 126 (90 per cent) of those who were anti‐HBs positive, but in none who were HBsAg and anti‐HBs negative. The highest titers of anti‐HBc, both among blood donors and patients with bleeding disorders occurred in those who were HBsAg positive. Among patients who were both anti‐HBs and anti‐HBc positive, highest anti‐HBc titers occurred in those aged 31 to 40. Anti‐e was detected in 59 per cent of HBsAg positive and 5 per cent of anti‐HBs positive blood donors, but e‐antigen was detected in none.

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Of 33 patients with acute hepatitis in Malawi, 21 had infection by hepatitis-B virus (HBV), five by hepatitis-A virus (HAV) and seven, who had no markers of current HBV or HAV infections, were probably infected by the agent(s) of non-A, non-B, hepatitis. 87 of 88 sera from persons without liver disease contained antibody to HAV and 49 antibody to hepatitis-B surface antigen (anti-HBs) (six were positive for hepatitis-B surface antigen). The diagnosis of recent infection by HAV was made by detecting HAV-specific IGM in single serum samples and, although such tests showed that HAV caused acute hepatitis, its absence in patients with chronic liver disease suggests that, unlike HBV, infection by HAV does not play a role in chronic liver disease in Malawi. Anti-hepatis-B core antigen (anti-HBc)-specific IgM was detected in 19 of 21 patients with acute HBV infection, in three of five HbsAg-positive patients with cirrhosis, but in none of five HbsAg-positive patients with hepatoma.