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129 blood donors found to be HBsAg-positive on routine testing were studied for evidence of hepatic disease. Twelve had already lost the antigen from the serum when histologically examined. None of these has had clinical or histological evidence of inflammatory liver disease. Two of the 129 patients showed mild icteric hepatitis, cleared the antigen during the follow up and became anti-HBs positive. The remaining 115 patients who appeared clinically healthy and who had no history of previous icteric liver disease remained HBsAg positive during a mean follow up period of 17.3 +/- 3.0 months. Forty patients from these had a normal liver histology and 37 mild to distinct steatosis but no signs of inflammatory liver disease. 11 patients a mild nonspecific mesenchymal activity but no focal necrosis, 16 patients had mild infiltration in portal tracts and a few necrotic parenchymal cells with mesenchymal reaction, 6 patients had chronic persistent hepatitis, 4 chronic aggressive hepatitis, and 1 definite posthepatic cirrhosis.

Family members of 34 asymptomatic HBsAg carriers were tested for different hepatitis B virus (HBV) markers. Among 67 family members tested 24 (36%) presented signs of a past or ongoing HBV-infection. Spread of HBV-infection was particularly high in those families in which the HBsAg carrier was positive for HBeAg and Dane particle-associated DNA polymerase activity. Non-parenteral "horizontal" transmission of HBV among spouses and brothers and sisters and probably parenteral vertical transmission of HBV from carrier mothers to their infants occurred in approximately the same frequency. Fathers transmitted HBV unfrequently to their offsprings. The results show that the risk to acquire a HBV-infection from an asymptomatic HBsAg carrier is closely linked to the serological findings in the HBe/anti-HBe-system of the index HBsAg carrier and not to the family relationship to the HBsAg carrier.