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American Liver Foundation
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New York, New York 10006
Hans Popper Memorial Postdoctoral Research Fellowship
Gladstone Institutes, San Francisco, California
Role of Lipid Droplets in Hepatitis C Virus Infection and Liver Damage
The goal of Dr. Camus’s proposal is to characterize molecular mechanisms controlling Hepatitis C Virus (HCV) replication at lipid droplets (LDs) and leading to liver damages in infected patients. LDs have emerged as central cellular organelles in HCV replication. Triglycerides stored in LDs can be generated by two diacylglycerol acyltransferase (DGAT) enzymes.
Recent results from his laboratory indicate that HCV exclusively replicates at LDs generated by DGAT1. To define the role of DGAT1 in HCV replication, Dr. Camus will 1) characterize proteins interacting specifically with DGAT1 or DGAT2 in hepatoma cells to identify factors that favour or disfavour HCV particle production associated with DGAT1 or DGAT2 respectively. 2) His preliminary results show that two HCV proteins, core and NS5A, interact physically with DGAT1. He will perform a mutagenesis study of DGAT1 and these viral factors to elucidate the role of their interactions in viral assembly. 3) Transgenic mice expressing core develop fatty liver/steatosis, a frequent symptom in HCV-infected individuals. To examine whether DGAT1-generated LDs play a role in core-induced steatosis, he will generate core-transgenic mice in a DGAT1-/- background.
Dr. Camus anticipates that these studies will provide important new insight into the HCV life cycle at LDs and will determine whether DGAT1 is a novel antiviral drug target in HCV infection.