Cdc42 – A tryst between host cholesterol metabolism and infection

Dmitri Sviridov, Nigora Mukhamedova

Research output: Contribution to journalArticleOtherpeer-review

Abstract

Emerging evidence points to an important connection between pathogenesis of intracellular infections and host cholesterol metabolism. In our study we demonstrated that human cytomegalovirus exploits host small GTPase Cdc42 to hijack cellular cholesterol efflux pathway. It appears that the virus uses host machinery to stimulate cholesterol efflux by modifying lipid rafts and altering properties of plasma membrane, but the altered pathway is controlled by the viral protein US28 instead of the host ATP binding cassette transporter A1. We speculate that virus-controlled remodeling of plasma membrane facilitates immune evasion, exocytosis of viral proteins and cell-to-cell transmission of human cytomegalovirus. These mechanisms may be not unique for the cytomegalovirus and subverting reverse cholesterol transport pathway may be a generic mechanism used by pathogens to alter properties of host plasma membrane adapting it for their purposes—to hide and disseminate.

Original languageEnglish
Pages (from-to)237-241
Number of pages5
JournalSmall GTPases
Volume9
Issue number3
DOIs
Publication statusPublished - 2018
Externally publishedYes

Keywords

  • ABCA1
  • cholesterol efflux
  • HCMV
  • intracellular pathogens
  • lipid microdomains
  • lipid rafts

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