期刊
CELL HOST & MICROBE
卷 8, 期 5, 页码 422-432出版社
CELL PRESS
DOI: 10.1016/j.chom.2010.10.006
关键词
-
资金
- NIH [T32 AI065382-01]
- Region V Great Lakes RCE (NIH) [1-U54-AI-057153]
Autophagy influences numerous cellular processes, including innate and adaptive immunity against intracellular pathogens. However, some viruses, including dengue virus (DENV), usurp autophagy to enhance their replication. The mechanism for a positive role of autophagy in DENV infection is unclear. We present data that DENV induction of autophagy regulates cellular lipid metabolism. DENV infection leads to an autophagy-dependent processing of lipid droplets and triglycerides to release free fatty acids. This results in an increase in cellular beta-oxidation, which generates ATP. These processes are required for efficient DENV replication. Importantly, exogenous fatty acids can supplant the requirement of autophagy in DENV replication. These results define a role for autophagy in DENV infection and provide a mechanism by which viruses can alter cellular lipid metabolism to promote their replication.
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