*Mankgopo M. Kgatle, Mashiko Setshedi
Department of Medicine, Faculty of Health Sciences, University of Cape Town and Groote Schuur Hospital, Cape Town, South Africa
*Correspondence to firstname.lastname@example.org
Disclosure: The authors have declared no conflicts of interest.
Received: 01.02.16 Accepted: 23.03.16
Citation: EMJ Hepatol. 2016;4:84-92.
Chronic hepatitis B (CHB) is a serious consequence of hepatitis B virus (HBV), which infects and replicates in the liver. It is characterised by prolonged hepatitis B surface antigen seropositivity; this can lead to both cirrhosis and hepatocellular carcinoma (HCC). The infection begins when HBV binds its only known functional receptor, sodium taurocholate cotransporting polypeptide (NTCP), which was identified recently. The discovery of NTCP was a significant breakthrough in the field of HBV research, and has facilitated the establishment of a susceptible hepatoma cell line model for studying the mechanisms underlying HBV pathogenesis. Following productive HBV infection, both cellular and humoral immune cells and molecules, such as T cells and chemokines, are activated to resolve infection by destroying HBV-infected hepatocytes. However, host immunity to HBV is not always protective, most likely due to immune evasion mechanisms employed by HBV. These mechanisms may result in viral persistence, accumulation of mutations, and aberrant epigenetic alterations that lead to HCC. Here we highlight our current understanding of the HBV replication cycle, immunopathogenesis, and related mechanisms underlying the progression of CHB to advanced liver disease, along with the attendant complications.