Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.antiviral.2011.11.014
Title: U18666A, an intra-cellular cholesterol transport inhibitor, inhibits dengue virus entry and replication
Authors: Poh, M.K.
Shui, G. 
Xie, X.
Shi, P.-Y.
Wenk, M.R.
Gu, F.
Keywords: Antiviral
Cholesterol
Dengue virus
Fatty acids
U18666A
Issue Date: Jan-2012
Citation: Poh, M.K.,Shui, G.,Xie, X.,Shi, P.-Y.,Wenk, M.R.,Gu, F. (2012-01). U18666A, an intra-cellular cholesterol transport inhibitor, inhibits dengue virus entry and replication. Antiviral Research 93 (1) : 191-198. ScholarBank@NUS Repository. https://doi.org/10.1016/j.antiviral.2011.11.014
Abstract: 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. © 2011 Elsevier B.V.
Source Title: Antiviral Research
URI: http://scholarbank.nus.edu.sg/handle/10635/117211
ISSN: 01663542
DOI: 10.1016/j.antiviral.2011.11.014
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