Journal article

Publication year: 2015

Pages: 1-10

Journal: Hepatobiliary Surgery and Nutrition

Volume number: 4

Issue number: 1

ISSN: 2304-3881

eISSN: 2304-389X

DOI Link: https://doi.org/10.3978/j.issn.2304-3881.2014.12.08

Publisher: AME Publishing

Abstract: 
Chronic infection with hepatitis B virus (HBV) is the leading cause of liver cirrhosis and hepatocellular carcinoma worldwide. HBV life cycle begins with viral attachment to hepatocytes, mediated by the large HBV surface protein (LHBs). Identification of the sodium-taurocholate cotransporting polypeptide (NTCP) as a HBV receptor has revealed a suitable target for viral entry inhibition. Analysis of serum hepatitis B surface antigen (HBsAg) level is a non-invasive diagnostic parameter that improves HBV treatment opportunities. Furthermore, HBsAg plays an important role in manipulation of host immune response by HBV. However, observations in patients with chronic hepatitis B under conditions of immune suppression and in transgenic mouse models of HBV infection suggest, that in absence of adaptive immune responses 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 options modulating associated biological implications.

Harvard Citation style: Churin, Y., Roderfeld, M. and Roeb, E. (2015) Hepatitis B virus large surface protein: function and fame, Hepatobiliary surgery and nutrition, 4(1), pp. 1-10. https://doi.org/10.3978/j.issn.2304-3881.2014.12.08

APA Citation style: Churin, Y., Roderfeld, M., & Roeb, E. (2015). Hepatitis B virus large surface protein: function and fame. Hepatobiliary surgery and nutrition. 4(1), 1-10. https://doi.org/10.3978/j.issn.2304-3881.2014.12.08