Hepatitis B virus infection in the acquired immunodeficiency syndrome

The relationship between the immune deficiency and the attendant opportunistic infections and neoplasms may lead to fundamental clues about the role of the immune system in health and disease. The populations that are at high risk for the development of this syndrome are also at high risk of developing hepatitis B virus infection. This observation has led to the suggestion that hepatitis B virus may play an etiologic or contributory role in the development of the acquired immunodeficiency syndrome. We have evaluated the serologic and serum biochemical evidence of acute and chronic hepatitis B virus infection from 30 patients with the acquired immunodeficiency syndrome who were treated at the National Institutes of Health ove a 2-year period. Sera from 23 and 24 patients were positive for anti-HBs and anti-HBc, respectively. Only 3 patients (2 Haitians and 1 homosexual man) were seronegative for all hepatitis B virus markers. Three other patients were HBsAg-positive, all of whom appeared to be chronic HBsAg carriers. Two of these patients were also reactive for HBeAg, hepatitis B virus-DNA, and DNA polymerase activity. The remaining carrier was seropositive for anti-HBe and had no detectable hepatitis B virus DNA or DNA polymerase in serum. Serum aminotransferase levels were mildly elevated (less than twice the upper limit of the normal range) in the two patients with HBeAg. Results of other biochemical tests of liver function were normal. No patient had antibody to delta antigen. Hepatitis B virus infection is common in patients who develop the acquired immunodeficiency syndrome, but serious or progressive chronic hepatitis due to this virus is rare. Although 90% of patients had serologic evidence of hepatitis B virus infection, only 10% were seropositive for HBsAG and all of the antigen-positive patients had minimal evidence of chronic liver disease and none had antibody to delta antigen. Patients with the acquired immunodeficiency syndrome, despite having evidence of hepatitis B virus replication, have little evidence of an accompanying hepatitis. This observation suggests that chronic type B hepatitis is dependent on an immune response to viral replication, and in patients with the acquired immunodeficiency syndrome with chronic hepatitis B virus infection there is an unopposed replication of virus, similar to that seen with herpes simplex and cytomegalovirus. Thus, the immunologic deficiencies associated with the acquired immunodeficiency syndrome may well lead to an improvement in the biochemical and histological features of chronic type B hepatitis.