Journal
NATURE MEDICINE
Volume 16, Issue 11, Pages 1295-1298Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nm.2238
Keywords
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Funding
- Gladstone Institutes
- Hellman Family Foundation
- US National Institutes of Health [R03 AI069090, R01 DK056084, P30 DK026743]
- Human Frontiers Science Program
- Agence nationale de recherches sur le sida et les hepatites virales
- US National Institute of Diabetes and Digestive and Kidney Diseases
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Hepatitis C virus (HCV) infection is closely tied to the lipid metabolism of liver cells. Here we identify the triglyceride-synthesizing enzyme diacylglycerol acyltransferase-1 (DGAT1) as a key host factor for HCV infection. DGAT1 interacts with the viral nucleocapsid core and is required for the trafficking of core to lipid droplets. Inhibition of DGAT1 activity or RNAi-mediated knockdown of DGAT1 severely impairs infectious virion production, implicating DGAT1 as a new target for antiviral therapy.
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