Hub members Have many expertise, covering most of the fields in bioinformatics and biostatistics. You'll find below a non-exhaustive list of these expertise
Searched keyword : Hepatitis B virus (HBV)
Related people (0)Sorry nobody has this skill yet...
Related projects (2)
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.
According to the WHO, the Hepatitis B virus (HBV) infects chronically 295 million persons. After several decades, persistently infected patients become at risk to develop liver cirrhosis and/or liver cancer (hepatocellular carcinoma, HCC). Each year around one million persons die from these two complications directly triggered by HBV. In the course of infection, the HBV DNA genome accumulates mutations that become progressively dominant. Some of the recurrent mutations are suspected to play a significant role in the pathophysiology of liver disease by changing the biological activity of HBV-encoded genes or proteins. However, the virus is rarely acting alone to promote terminal liver diseases, and its deleterious activity is generally potentialized by other risk factors concomitant to viral presence. It is the case of alcohol or tobacco consumption, metabolism-associated fatty liver disease, herbal medicine containing aristolochic acid, or mycotoxin-contaminated food. Most of these agents are known to leave mutation fingerprints on the human genome. However, we do not currently know whether these mutagens contribute or not to the mutational burden observed on HBV DNA after decades of infection. We hypothesize that it could be the case. The characterization of the full mutation spectrum of the HBV genome including the application of tools initially proposed to analyze human mutations is the aim of this research program.