Treatment of Chronic Hepatitis B Virus Infection in Patients Co-infected with Hiv

Chronic infection with hepatitis B virus (HBV) affects about 5% of the world population (1). In Western Europe, Australia and the USA prevalence of chronic carriers of hepatitis B surface antigen (HBsAg) is less than 1% of the population. Among human immunodeficiency virus (HIV) infected individuals this prevalence is approximately 10 fold higher (2). Until recently, studies on HBV infection in HIV seropositive patients have not been emphasized. The natural history of chronic HBV infection is modified by co-infection with HIV. After initial HBV infection, both development and persistence of chronic HBV infection are greater in patients with prior HIV infection (3, 4). Among chronic hepatitis B surface antigen (HBsAg) carriers a high level of HBV replication or the presence of hepatitis B e antigen (HBeAg) are common in HIV/HBV co-infected individuals (3, 4). These 2 conditions may be predictive of poor survival. However, studies performed prior to the era of highly active antiretroviral therapy (HAART) (prior to 1997), found mild necroinflammatory liver lesions associated with low serum transaminases in deeply immunossupressed HIV/HBV co-infected patients (5-8). More recent studies, conducted in HAART era, have reported a higher incidence rate of liver related cirrhosis and mortality in HIV/HBV co-infected patients compared to HIV mono-infected persons (9, 10). Factors impacting progression to cirrhosis in HIV/HBV co-infected patients remain unknown. HAART-related immune restoration may have switched the immune reaction to HBV from a tolerance to an intolerance phase, leading in some cases to the complete control of HBV replication or in a majority of patients to an exacerbation of chronic hepatitis. HAART-related hepatotoxicity could also have contributed to worsening of liver damage. On the other hand, improvement of liver lesions may be observed in patients receiving antiretroviral regimens containing lamivudine. Finally, the effect of HIV infection on the natural history of chronic hepatitis B (CHB) could also have been modified by a longer life expectancy, which may allow greater time for cirrhosis to develop. Studies of the natural history of CHB are needed to identify which patients may have the greater benefit from anti-HBV therapy, and to assess when to treat. Therefore, due to the complex potent interactions between these two viruses, the immune system and antiretroviral therapy, the strategy and management of anti-HBV therapy in HIV-infected persons must take into consideration both virus infections.