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Searched keyword : Hepatitis B virus (HBV)
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Despite effective prevention against HBV infection, 300 million people worldwide are chronic HBV carriers, of whom 25% will die of liver cirrhosis or hepatocellular carcinoma (HCC). Current treatments for chronic hepatitis B (CHB) are inefficient to completely clear the virus and liver cancer is a lethal disease, thus representing an area of highly unmet medical need. Viral persistence is due to the maintenance, in the nuclei of infected cells, of the viral nuclear DNA : the cccDNA that is not targeted by the antiviral treatment and to the impairment of both the innate and adaptive immune responses that accompanies CHB infection. Viral replication depends on a balance between factors that benefit and those that restrict viral infection. However little is known about cellular factors that repress HBV replication. Using quantitative temporal viromics approach developed by P. Lenher in Cambridge we have performed a quantitative analysis of temporal changes in host and viral proteins in primary human hepatocytes through the course of HBV infection. We will in particular search for cellular factors involved in virus restriction and uncover the mechanism of viral escape.