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

Research output: Contribution to journalArticle

67 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)191-198
Number of pages8
JournalAntiviral research
Issue number1
StatePublished - Jan 1 2012



  • Antiviral
  • Cholesterol
  • Dengue virus
  • Fatty acids
  • U18666A

ASJC Scopus subject areas

  • Pharmacology
  • Virology

Cite this