Mechanisms of Cell-to-Cell Transfer of HIV-1 toward Myeloid Cells

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Immunological Responses and Immune Defense Mechanisms".

Deadline for manuscript submissions: closed (15 November 2021) | Viewed by 6013

Special Issue Editors


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Guest Editor
Institute of Pharmacology and Structural biology (IPBS), CNRS-University of Toulouse, 31077 Toulouse, France
Interests: cell biology; cell cytoskeleton; macrophages; osteoclasts; HIV-1; HIV/Mtb co-infection

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Guest Editor
Sir William Dunn School of Pathology, Oxford University, Oxford OX1 3RE, UK
Interests: HIV-1; cell-to-cell virus transfer; macrophages

Special Issue Information

Dear Colleagues,

Myeloid cells, including macrophages and dendritic cells, as well as bone osteoclasts,  are cellular targets of HIV-1 that play crucial roles in the physiopathology of infection as well as in virus dissemination and establishment of persistent virus reservoirs in numerous host tissues. While myeloid cells are poorly infected in vitro by cell-free viruses, cell-to-cell transfer of HIV-1 likely represents the dominant mode of virus dissemination in vivo and may allow for productive infection of these cell types. Thus, studying HIV-1 cell-to-cell transfer mechanisms toward myeloid cells is essential to better understand the pathogenesis of the disease and to prevent establishment of viral reservoirs.  

Therefore, for this Special Issue of Pathogens, we invite you to submit your contributions in the form of original research articles, reviews, and short communications about cell-to-cell transfer of HIV-1 involving myeloid cells.

Dr. Christel Verollet
Dr. Maeva Dupont
Guest Editors

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Keywords

  • HIV-1
  • cell-to-cell viral transfer
  • macrophages
  • dendritic cells

Published Papers (2 papers)

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Research

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28 pages, 3672 KiB  
Article
Embedding of HIV Egress within Cortical F-Actin
by Anupriya Aggarwal, Alberto Ospina Stella, Catherine C. Henry, Kedar Narayan and Stuart G. Turville
Pathogens 2022, 11(1), 56; https://doi.org/10.3390/pathogens11010056 - 3 Jan 2022
Cited by 7 | Viewed by 2793
Abstract
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 [...] Read more.
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. Full article
(This article belongs to the Special Issue Mechanisms of Cell-to-Cell Transfer of HIV-1 toward Myeloid Cells)
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Review

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14 pages, 820 KiB  
Review
HIV-1 trans-Infection Mediated by DCs: The Tip of the Iceberg of Cell-to-Cell Viral Transmission
by Daniel Perez-Zsolt, Dàlia Raïch-Regué, Jordana Muñoz-Basagoiti, Carmen Aguilar-Gurrieri, Bonaventura Clotet, Julià Blanco and Nuria Izquierdo-Useros
Pathogens 2022, 11(1), 39; https://doi.org/10.3390/pathogens11010039 - 31 Dec 2021
Cited by 4 | Viewed by 2705
Abstract
HIV-1 cell-to-cell transmission is key for an effective viral replication that evades immunity. This highly infectious mechanism is orchestrated by different cellular targets that utilize a wide variety of processes to efficiently transfer HIV-1 particles. Dendritic cells (DCs) are the most potent antigen [...] Read more.
HIV-1 cell-to-cell transmission is key for an effective viral replication that evades immunity. This highly infectious mechanism is orchestrated by different cellular targets that utilize a wide variety of processes to efficiently transfer HIV-1 particles. Dendritic cells (DCs) are the most potent antigen presenting cells that initiate antiviral immune responses, but are also the cells with highest capacity to transfer HIV-1. This mechanism, known as trans-infection, relies on the capacity of DCs to capture HIV-1 particles via lectin receptors such as the sialic acid-binding I-type lectin Siglec-1/CD169. The discovery of the molecular interaction of Siglec-1 with sialylated lipids exposed on HIV-1 membranes has enlightened how this receptor can bind to several enveloped viruses. The outcome of these interactions can either mount effective immune responses, boost the productive infection of DCs and favour innate sensing, or fuel viral transmission via trans-infection. Here we review these scenarios focusing on HIV-1 and other enveloped viruses such as Ebola virus or SARS-CoV-2. Full article
(This article belongs to the Special Issue Mechanisms of Cell-to-Cell Transfer of HIV-1 toward Myeloid Cells)
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