Hepatitis B viral infection.
Although the strategy of replication of hepatitis B virus has now been described, the majority of the compounds that have activity against the virus have been identified by empirical means. Vidarabine, acyclovir, and interferons alpha and beta are capable of inhibiting hepatitis B virus replication; however, at the present time, optimal treatment regimens have not been defined. The effects of interferons alpha and beta given in short courses are only transient. Longer courses of intermittent therapy have resulted in seroconversion rates of up to 50 percent in Western European carriers. It is becoming apparent that patients infected with hepatitis B virus in adult life have a relative deficiency of interferon alpha, and it is these patients who have the best responses to protracted courses of intermittent therapy.
D000212:Acyclovir / Q000627:therapeutic use*; D000328:Adult; D006509:Hepatitis B / Q000628:therapy*; D006801:Humans; D007231:Infant, Newborn; D007370:Interferon Type I / Q000627:therapeutic use*; D007371:Interferon-gamma / Q000627:therapeutic use; D007376:Interleukin-2 / Q000627:therapeutic use; D011239:Prednisolone / Q000627:therapeutic use; D011994:Recombinant Proteins / Q000627:therapeutic use; D014740:Vidarabine / Q000627:therapeutic use*
D007370:Interferon Type I; D007376:Interleukin-2; D011994:Recombinant Proteins; D007371:Interferon-gamma; D011239:Prednisolone; D014740:Vidarabine; D000212:Acyclovir