Hepatitis B virus (HBV) markers were measured in 83 immunosuppressed renal transplant patients who were followed for periods of 2 to 15 years. Sixty-nine patients were negative for HBsAg before transplantation, of whom 14 were positive for anti-HBs. The remaining 14 patients were HBsAg positive prior to transplantation. Eighteen patients were identified as being HBsAg positive during the follow-up period. Four patients acquired primary type B hepatitis; one died of submassive hepatic necrosis and the remaining three became chronic HBV carriers with positive HBeAg, DNA polymerase, and HBV DNA. Several patterns of HBV expression were observed in HBsAg-positive patients. Four patients were HBsAg, HBeAg, DNA polymerase, and HBV DNA positive prior to transplantation, and these markers persisted. Reactivation of HBV replication occurred in eight patients, seven of whom were HBsAg positive and HBeAg and anti-HBe negative originally; one patient was anti-HBc positive. A single patient was HBsAg and anti-HBe positive and remained so for 22 months. The remaining previously HBsAg-positive patient is currently HBsAg negative. These serological data suggest that reactivation of HBV replication or continued hepatitis B virion replication occurs as commonly or more commonly than de nouo infection in renal transplant recipients. The presence of HBeAg in serum predisposes to long-term Dane particle expression in immunosuppressed patients, whereas anti-HBe-positive carriers may not always be susceptible to reactivation of HBV replication despite immunosuppression.Several viral infections are potentiated in immunocompromised hosts. Cytomegalovirus, herpes simplex, varicella-zoster, and Epstein Barr virus infection occur with increased frequency in immunosuppressed renal transplant recipients (1). Patients with chronic renal failure on maintainance hemodialysis and renal transplant recipients are particularly liable to chronic hepatitis B virus (HBV) infection (2, 3). Viral replication is favored in azotemic hemodialysis patients, and they are frequently hepatitis B e antigen (HBeAg) positive and HBV DNA polymerase positive (4).Reactivation of type B hepatitis may follow treatment with immunosuppressive drugs and chemotherapy. Reappearance of HBsAg in serum of HBsAg-negative

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