Viral hepatitis: virus/host interaction

Abstract

Abstract Hepatitis A virus is considered directly cytopathic to the liver cell. Severity of the liver damage is dictated by viral load. Acute infection is followed by sustained immunity to the virus. Hepatitis B (HBV) and C (HCV) viruses are noncytopathic, hepatotropic viruses that cause acute and chronic hepatitis and hepatoma. Cellular and humoral immune responses are responsible not only for viral clearance but also for hepatocyte damage. T‐cell response to HBV is vigorous, polyclonal, and multispecific in acutely infected patients who clear the virus while it is weak and narrowly focused in chronically infected patients. It is mainly executed by cytotoxic T lymphocytes (CTL), which destroy infected hepatocytes and secrete antiviral cytokines that interrupt the HBV life cycle. T‐cell response to HCV is strong and multispecific in both acutely and chronically infected patients. Whether HCV is susceptible to a cytokine‐mediated type of control is unknown. The ability of HCV to persist despite a strong CTL response suggests that HCV is either less visible to the CTL or less responsive to cytokine‐mediated antiviral signals than HBV. Both viruses, but especially HCV, have a high mutation rate, leading to the occurrence of variant viral genomes with growth advantage and the ability of escaping immune recognition.