High frequency of hepatitis B virus DNA in anti-HBe positive sera on longitudinal follow-up of patients with renal transplants and chronic hepatitis B

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Abstract
Hepatitis B virus (HBV) markers were determined in 821 patients receiving renal allografts and undergoing immunosuppressive therapy during 1970–1986. Twenty‐four of the patients with a renal transplant functioning for longer than 1 year originally were or became chronic carriers of hepatitis B surface antigen (HBsAg). These patients remained carriers during the follow‐up period, which lasted until death or until the end of 1986. Follow‐up time was 1.2–15.3 years (mean 9.1 years). A total of 301 samples from the HBsAg‐positive patients were tested for HBV DNA and HBeAg/DNA and HBeAg/anti‐HBe. Nine patients who were constantly positive for HBeAg also remained positive for HBV DNA. Reactivation of HBV replication occurred in 11 patients. Among these, HBV DNA and HBeAg varied in parallel in six patients, three patients developed anti‐HBe, and two patients were constantly positive for anti‐HBe. Another four of the 24 patients seroconverted to anti‐HBe, and two of these also lost HBV DNA. Three of 12 deceased patients died from liver failure during follow‐up. None of these three had been constantly positive for HBeAg or HBV DNA, but they had had reactivations of HBV; two were also positive for HBV DNA in serum specimens available from their terminal month. HBV DNA was demonstrated in 99% of HBeAgpositive and 53% of anti‐HBe‐positive sera and in at least two samples from each of the 24 patients. It may be presumed that the reason for failure to eliminate the HBV infection, and for progressive liver disease in this group of patients, was a discordant T‐and B‐cell response to HBeAg. Due to the high frequency of HBV DNA in HBeAg negative and in anti‐HBe positive sera from immunosuppressed HBsAg‐positive renal transplant patients, determination of serum HBV DNA is important for defining infectivity in these patients.