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Inhibiting the Ins and Outs of HIV replication: Cell-intrinsic antiretroviral restrictions at the plasma membrane

Research output: Contribution to journalReview articlepeer-review

Original languageEnglish
Article number1853
JournalFrontiers in Immunology
Volume8
Issue numberJAN
DOIs
Accepted/In press7 Dec 2017
Published4 Jan 2018

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  • Inhibiting the Ins and Outs_FOSTER_Published4January2018_GOLD VoR (CC BY)

    Inhibiting_the_Ins_and_Outs_FOSTER_Published4January2018_GOLD_VoR_CC_BY_.pdf, 1.83 MB, application/pdf

    Uploaded date:16 Jan 2018

    Version:Final published version

    Licence:CC BY

    Copyright © 2018 Foster, Pickering and Neil. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

King's Authors

Abstract

Like all viruses, human immunodeficiency viruses (HIVs) and their primate lentivirus relatives must enter cells in order to replicate and, once produced, new virions need to exit to spread to new targets. These processes require the virus to cross the plasma membrane of the cell twice: once via fusion mediated by the envelope glycoprotein to deliver the viral core into the cytosol; and secondly by ESCRT-mediated scission of budding virions during release. This physical barrier thus presents a perfect location for host antiviral restrictions that target enveloped viruses in general. In this review we will examine the current understanding of innate host antiviral defences that inhibit these essential replicative steps of primate lentiviruses associated with the plasma membrane, the mechanism by which these viruses have adapted to evade such defences, and the role that this virus/host battleground plays in the transmission and pathogenesis of HIV/AIDS.

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