Journal
ANTIVIRAL RESEARCH
Volume 93, Issue 1, Pages 191-198Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.antiviral.2011.11.014
Keywords
Dengue virus; Cholesterol; Antiviral; Fatty acids; U18666A
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Funding
- Singapore National Research Foundation under CRP [2007-04]
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The level of cholesterol in host cells has been shown to affect viral infection. However, it is still not understood why this level of regulation is important for successful infection. We have shown in this study that dengue virus infection was affected when the cholesterol intake in infected cells was disrupted using a cholesterol transport inhibitor, U18666A. The antiviral effect was found to result from two events: retarded viral trafficking in the cholesterol-loaded late endosomes/lysosomes and suppressed de novo sterol biosynthesis in treated infected cells. We also observed an additive antiviral effect of U18666A with C75, a fatty acid synthase inhibitor, suggesting dengue virus relies on both the host cholesterol and fatty acid biosynthesis for successful replication. (C) 2011 Elsevier B.V. All rights reserved.
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