U18666A, an intra-cellular cholesterol transport inhibitor, inhibits dengue virus entry and replication.

Mee Kian Poh, Guanghou Shui, Xuping Xie, Pei-Yong Shi, Markus R Wenk, Feng Gu

Dengue Unit, Novartis Institute for Tropical Diseases, 10 Biopolis Road, Chromos #05-01, Singapore 138670, Singapore.

Antiviral research 2012 Jan

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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. Copyright © 2011 Elsevier B.V. All rights reserved.

Citation

Mee Kian Poh, Guanghou Shui, Xuping Xie, Pei-Yong Shi, Markus R Wenk, Feng Gu. U18666A, an intra-cellular cholesterol transport inhibitor, inhibits dengue virus entry and replication. Antiviral research. 2012 Jan;93(1):191-8