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HIV-1 trans-Infection Mediated by DCs: The Tip of the Iceberg of Cell-to-Cell Viral Transmission

Embedding of HIV Egress within Cortical F-Actin

The Kirby Institute, University of New South Wales, Sydney, NSW 2052, Australia
Center for Molecular Microscopy, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
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;
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.

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.

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.

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