Biology and molecular pathogenesis of hepatitis B virus infection

Abstract

Hepatitis B virus (HBV) remains a global public health infection. Over the past several decades, the basic principles of HBV gene expression and replication as well as the viral and host determinants governing infection outcomes have been largely uncovered. The clinical manifestations of HBV infection vary from an acute and chronic form of the disease. During the acute phase of the infection, the disease manifestations vary from subclinical hepatitis to anicteric hepatitis, icteric hepatitis, and fulminant hepatitis while during the chronic infection, manifest in different from ranging from asymptomatic carrier state to chronic hepatitis, cirrhosis, and hepatocellular carcinoma. The clinical outcome of the infection depends upon the level of HBV replication, age at infection, and the immune status of the host. HBV integration into the host genome often serves as a relevant source of hepatitis B surface antigen (HBsAg) expression during chronic infection, possibly triggering an immune response. If HBV is not eliminated, a delicate balance between viral replication and immune defence prevails which may lead to chronic hepatitis and liver cirrhosis. It is generally acknowledged that the humoral antibody response contributes to the clearance of circulating virus particles and the prevention of viral spread within the host while the cellular immune response eliminates infected cells.