Infection with the human immunodeficiency virus (HIV) modifies the course of infection by the virus of hepatitis B (HBV) by several mechanisms: the rate of chronicity, prolonging viremia by HBV, and increase in morbidity related to liver disease. The treatment for both infections should be done in a coordinated manner, to avoid the emergence of resistance in HIV, HBV or both, as well as major alterations in the hepatic enzymes. Monotherapies with lamivudine or emtricitabine select, rapidly, mutant strains of the HBV and HIV. Monotherapy with adefovir has moderate effects in coinfected patients as they already have mutations. If the treatment of HBV can defer until the combination antiretroviral therapy of HIV is necessary, these patients should receive a combination of tenofovir plus lamivudine (or emtricitabine), since this provides a powerful therapy against HBV and establishes a good central axis for antiretroviral therapy. In addition, it would prevent the selection of HBV variant resistance. The influence of HIV in the HCV infection. Increase in load HIV-driven viral hepatitis exacerbates hepatic lesions and influences transmission of the HCV. The risk of sexual transmission increases when HIV is present in the carrier. Coinfection modifies the evolution of fibrosis in patients with HIV, with higher speed in those who have low CD4 counts, so that the onset of cirrhosis occurs before, and the risk of liver decompensation is also more frequent. The consequence of this situation is an increase in liver-related morbidity and mortality.
Part of the book: Hepatitis B and C