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American Society for Microbiology, Journal of Virology, 4(83), p. 2044-2047, 2009

DOI: 10.1128/jvi.01876-08

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Cyclophilin A Levels Dictate Infection Efficiency of Human Immunodeficiency Virus Type 1 Capsid Escape Mutants A92E and G94D

Journal article published in 2008 by Laura M. J. Ylinen, Torsten Schaller ORCID, Amanda Price, Adam J. Fletcher ORCID, Mahdad Noursadeghi, Leo C. James, Greg J. Towers ORCID
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

ABSTRACT Cyclophilin A (CypA) is an important human immunodeficiency virus type 1 (HIV-1) cofactor in human cells. HIV-1 A92E and G94D capsid escape mutants arise during CypA inhibition and in certain cell lines are dependent on CypA inhibition. Here we show that dependence on CypA inhibition is due to high CypA levels. Restricted HIV-1 is stable, and remarkably, restriction is augmented by arresting cell division. Nuclear entry is not inhibited. We propose that high CypA levels and capsid mutations combine to disturb uncoating, leading to poor infectivity, particularly in arrested cells. Our data suggest a role for CypA in uncoating the core of HIV-1 to facilitate integration.