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The influence of HTLV‐III infection on the natural history of hepatitis B virus infection in male homosexual HBsAg carriers

The presence of antibodies to HTLV‐III and markers of active hepatitis B virus replication was examined in a longitudinal study of 33 consecutive male homosexual HBsAg carriers. The mean follow‐up time was 37 months (range = 4 to 109 months). All patients were initially hepatitis B virus DNA‐positiv...

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Bibliographic Details
Published in:Hepatology (Baltimore, Md.) Md.), 1987-01, Vol.7 (1), p.37-41
Main Authors: Krogsgaard, Kim, Lindhardt, Bjarne ÖRskov, Nielsen, Jens Ole, Andersson, Poul, Kryger, Peter, Aldershvile, Jan, Gerstoft, Jan, Pedersen, Court
Format: Article
Language:English
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Summary:The presence of antibodies to HTLV‐III and markers of active hepatitis B virus replication was examined in a longitudinal study of 33 consecutive male homosexual HBsAg carriers. The mean follow‐up time was 37 months (range = 4 to 109 months). All patients were initially hepatitis B virus DNA‐positive and HBeAg positive. Antibodies to HTLV‐III were detectable in eight patients while they were positive for both of these markers. One of them cleared hepatitis B virus DNA and seroconverted from HBeAg to anti‐HBe. This corresponds to an annual clearance/seroconversion rate of 4% (95% confidence limits = 0 to 15%). In two patients, antibodies to HTLV‐III appeared after clearance of hepatitis B virus DNA and HBeAg, and in one of them, hepatitis B virus DNA reappeared. Among the 25 patients negative for HTLV‐III antibodies, the annual hepatitis B virus DNA clearance rate was 20% and HBeAg to anti‐HBe seroconversion rate was 11% (95% confidence limits = 11 to 31% and 4 to 20 % respectively). The observed hepatitis B virus DNA clearance rates in the two groups were significantly different (p < 0.05). Disease activity, as determined by transaminase levels, was significantly lower in HTLV‐III infected individuals as compared to individuals without HTLV‐III infection (p < 0.05). Infection with HTLV‐III may extend the period of active viral replication or even reactivate hepatitis B virus replication and seems to diminish inflammatory disease activity in chronic HBsAg carriers.
ISSN:0270-9139
1527-3350
DOI:10.1002/hep.1840070109