Hepatitis B virus large surface protein: function and fame

Chronic infection with hepatitis B virus (HBV) is the leading cause of liver cirrhosis andhepatocellular carcinoma worldwide. HBV life cycle begins with viral attachment to hepatocytes, mediatedby the large HBV surface protein (LHBs). Identification of the sodium-taurocholate cotransportingpolypeptide (NTCP) as a HBV receptor has revealed a suitable target for viral entry inhibition. Analysis ofserum hepatitis B surface antigen (HBsAg) level is a non-invasive diagnostic parameter that improves HBVtreatment opportunities. Furthermore, HBsAg plays an important role in manipulation of host immuneresponse by HBV. However, observations in patients with chronic hepatitis B under conditions of immunesuppression and in transgenic mouse models of HBV infection suggest, that in absence of adaptive immuneresponses cellular mechanisms induced by HBV may also lead to the development of liver diseases. Thus,the multifaceted pathological aspects of HBsAg predetermine the design of new therapeutical optionsmodulating associated biological implications.