Abstract

We suggest that subtle alterations in T-cell functions in male homosexuals makes them more likely to have silent anicteric hepatitis B infection, and perhaps more likely to become chronic carriers with significant chronic liver disease. This immunodeficiency might also explain why they respond less favourably to antiviral therapy. In future trials of antiviral therapy homosexual males should be randomised separately. Further studies of the immunomodulatory effects of new and existing agents will be of value in designing drug regimes particularly suited to the treatment of homosexual HBV carriers.

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