HBV pathogenesis in animal models: Recent advances on the role of platelets

Citations of this article
Mendeley users who have this article in their library.


Hepatitis B virus (HBV) causes acute and chronic necroinflammatory liver diseases and hepatocellular carcinoma (HCC). HBV replicates noncytopathically in the hepatocyte, and most of the liver injury associated with this infection reflects the immune response. While the innate immune response may not contribute significantly to the pathogenesis of liver disease or viral clearance, the adaptive immune response, particularly the cytotoxic T lymphocyte (CTL) response, contributes to both. Recent observations also reveal that antigen-nonspecific inflammatory cells enhance CTL-induced liver pathology and, more surprisingly, that platelets facilitate the intrahepatic accumulation of CTLs, suggesting that the host response to HBV infection is a highly complex but coordinated process. The notion that platelets contribute to liver disease and viral clearance by promoting the recruitment of virus-specific CTLs into the liver is a new concept in viral pathogenesis, which may prove useful to implement treatments of chronic HBV infection in man. © 2007 European Association for the Study of the Liver.




Iannacone, M., Sitia, G., Ruggeri, Z. M., & Guidotti, L. G. (2007, April). HBV pathogenesis in animal models: Recent advances on the role of platelets. Journal of Hepatology. https://doi.org/10.1016/j.jhep.2007.01.007

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free