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Curr Opin Virol. 2014 Feb;4:32-6. doi: 10.1016/j.coviro.2013.11.003. Epub 2014 Jan 14.

A model for cofactor use during HIV-1 reverse transcription and nuclear entry.

Author information

1
University College London, Medical Research Council Centre for Medical Molecular Virology, Division of Infection and Immunity, University College London, 90 Gower Street, London WC1E 6BT, United Kingdom.
2
University College London, Medical Research Council Centre for Medical Molecular Virology, Division of Infection and Immunity, University College London, 90 Gower Street, London WC1E 6BT, United Kingdom. Electronic address: g.towers@ucl.ac.uk.

Abstract

Lentiviruses have evolved to infect and replicate in a variety of cell types in vivo whilst avoiding the powerful inhibitory activities of restriction factors or cell autonomous innate immune responses. In this review we offer our opinions on how HIV-1 uses a series of host proteins as cofactors for infection. We present a model that may explain how the capsid protein has a fundamental role in the early part of the viral lifecycle by utilising cyclophilin A (CypA), cleavage and polyadenylation specificity factor-6 (CPSF6), Nup358 and TNPO3 to orchestrate a coordinated process of DNA synthesis, capsid uncoating and integration targeting that evades innate responses and promotes integration into preferred areas of chromatin.

PMID:
24525292
PMCID:
PMC3969716
DOI:
10.1016/j.coviro.2013.11.003
[Indexed for MEDLINE]
Free PMC Article

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