Cholesterol is required for infection by Semliki Forest virus

Thomas Phalen, Margaret Kielian

Research output: Contribution to journalArticle

136 Citations (Scopus)

Abstract

Semliki Forest virus (SFV) and many other enveloped animal viruses enter cells by a membrane fusion reaction triggered by the low pH within the endocytic pathway. In vitro, SFV fusion requires cholesterol in the target membrane, but the role of cholesterol in vivo is unknown. In this paper, the infection pathway of SFV was studied in mammalian and inset cells substantially depleted of sterol. Cholesteroldepleted cells were unaltered in their ability to bind, internalize, and acidify virus, but were blocked in SFV fusion and subsequent virus replication. Depleted cells could be infected by the cholesterol-independent vesicular stomatitis virus, which also enters cells via endocytosis and low pH-mediated fusion. The block in SFV infection was specifically reversed by cholesterol but not by cholestenone, which lacks the critical 3β-hydroxyl group. Cholesterol thus is central in the infection pathway of SFV, and may act in vivo to modulate infection by SFV and other pathogens.

Original languageEnglish (US)
Pages (from-to)615-623
Number of pages9
JournalJournal of Cell Biology
Volume112
Issue number4
StatePublished - Feb 1991

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Semliki forest virus
Cholesterol
Infection
Viruses
Cholestenones
Vesicular Stomatitis
Membrane Fusion
Sterols
Virus Diseases
Virus Replication
Endocytosis
Hydroxyl Radical
Cell Membrane
Membranes

ASJC Scopus subject areas

  • Cell Biology

Cite this

Cholesterol is required for infection by Semliki Forest virus. / Phalen, Thomas; Kielian, Margaret.

In: Journal of Cell Biology, Vol. 112, No. 4, 02.1991, p. 615-623.

Research output: Contribution to journalArticle

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