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Article

Embedding of HIV Egress within Cortical F-Actin

1
The Kirby Institute, University of New South Wales, Sydney, NSW 2052, Australia
2
Center for Molecular Microscopy, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
3
Cancer Research Technology Program, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA
*
Author to whom correspondence should be addressed.
Current address: David, H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Academic Editors: Christel Verollet and Maeva Dupont
Pathogens 2022, 11(1), 56; https://doi.org/10.3390/pathogens11010056
Received: 12 November 2021 / Revised: 22 December 2021 / Accepted: 28 December 2021 / Published: 3 January 2022
(This article belongs to the Special Issue Mechanisms of Cell-to-Cell Transfer of HIV-1 toward Myeloid Cells)
F-Actin remodeling is important for the spread of HIV via cell–cell contacts; however, the mechanisms by which HIV corrupts the actin cytoskeleton are poorly understood. Through live cell imaging and focused ion beam scanning electron microscopy (FIB-SEM), we observed F-Actin structures that exhibit strong positive curvature to be enriched for HIV buds. Virion proteomics, gene silencing, and viral mutagenesis supported a Cdc42-IQGAP1-Arp2/3 pathway as the primary intersection of HIV budding, membrane curvature and F-Actin regulation. Whilst HIV egress activated the Cdc42-Arp2/3 filopodial pathway, this came at the expense of cell-free viral release. Importantly, release could be rescued by cell–cell contact, provided Cdc42 and IQGAP1 were present. From these observations, we conclude that a proportion out-going HIV has corrupted a central F-Actin node that enables initial coupling of HIV buds to cortical F-Actin to place HIV at the leading cell edge. Whilst this initially prevents particle release, the maturation of cell–cell contacts signals back to this F-Actin node to enable viral release & subsequent infection of the contacting cell. View Full-Text
Keywords: HIV-1; HIV-1 Gag; CDC42; IQGAP1; ARP2/3; F-Actin; budding; Diaph2 HIV-1; HIV-1 Gag; CDC42; IQGAP1; ARP2/3; F-Actin; budding; Diaph2
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MDPI and ACS Style

Aggarwal, A.; Stella, A.O.; Henry, C.C.; Narayan, K.; Turville, S.G. Embedding of HIV Egress within Cortical F-Actin. Pathogens 2022, 11, 56. https://doi.org/10.3390/pathogens11010056

AMA Style

Aggarwal A, Stella AO, Henry CC, Narayan K, Turville SG. Embedding of HIV Egress within Cortical F-Actin. Pathogens. 2022; 11(1):56. https://doi.org/10.3390/pathogens11010056

Chicago/Turabian Style

Aggarwal, Anupriya, Alberto Ospina Stella, Catherine C. Henry, Kedar Narayan, and Stuart G. Turville. 2022. "Embedding of HIV Egress within Cortical F-Actin" Pathogens 11, no. 1: 56. https://doi.org/10.3390/pathogens11010056

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