After hepatitis B virus (HBV) infection, HBV DNA persists in minute amounts in hepatocyte nuclei even in individuals with "resolved" infection. Viral replication and development of liver disease depend on the balance between viral mechanisms promoting persistence and host immune control. Patients with active or inactive disease or resolved HBV infection are at risk for reactivation with immunosuppressive therapy use. HBV reactivation varies from a clinically asymptomatic condition to one associated with acute liver failure and death. We review recent studies on HBV reactivation during immunomodulatory therapies for oncologic, gastroenterological, rheumatic, and dermatologic disorders. Risk calculation should be determined through HBV screening and assessment of immunosuppressive therapy potency. We also discuss monitoring for reactivation, prophylactic antiviral therapy, and treatment of reactivation. Prophylactic antiviral treatment is needed for all HBsAg carriers and selected patients who have anti-HBc without HBsAg and is critical for preventing viral reactivation and improving outcomes.
Keywords: Chemotherapy; Entecavir; HBV DNA; Hepatitis B; Immunosuppression; Lymphoma; Prophylactic therapy; Reactivation; Rituximab.