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Trends Microbiol. 2019 Jun 28. pii: S0966-842X(19)30157-X. doi: 10.1016/j.tim.2019.06.002. [Epub ahead of print]

Molecular Mechanism of HIV-1 Entry.

Author information

1
Division of Molecular Medicine, Boston Children's Hospital, and Department of Pediatrics, Harvard Medical School, 3 Blackfan Street, Boston, MA 02115, USA. Electronic address: bchen@crystal.harvard.edu.

Abstract

HIV-1 envelope glycoprotein [Env; trimeric (gp160)3 cleaved to (gp120/gp41)3] attaches the virion to a susceptible cell and induces fusion of viral and cell membranes to initiate infection. It interacts with the primary receptor CD4 and coreceptor (e.g., chemokine receptor CCR5 or CXCR4) to allow viral entry by triggering large structural rearrangements and unleashing the fusogenic potential of gp41 to induce membrane fusion. Recent advances in structural biology of HIV-1 Env and its complexes with the cellular receptors have revealed molecular details of HIV-1 entry and yielded new mechanistic insights. In this review, I summarize our latest understanding of the HIV-1 membrane fusion process and discuss possible pathways for productive viral entry.

KEYWORDS:

HIV-1; envelope glycoprotein; membrane fusion; viral entry

PMID:
31262533
DOI:
10.1016/j.tim.2019.06.002

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