Journal
TRENDS IN MICROBIOLOGY
Volume 27, Issue 10, Pages 878-891Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.tim.2019.06.002
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Funding
- National Institutes of Health (NIH) [AI141002, AI106488, AI129721, AI127193]
- Collaboration for AIDS Vaccine Discovery (CAVD) [OPP1169339]
- Center for HIV/AIDS Vaccine Immunology - Immunogen Design [AI-100645]
- Bill and Melinda Gates Foundation [OPP1169339] Funding Source: Bill and Melinda Gates Foundation
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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.
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