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      HIV-1 Capture and Transmission by Dendritic Cells: The Role of Viral Glycolipids and the Cellular Receptor Siglec-1

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          Abstract

          Dendritic cells (DCs) are essential in order to combat invading viruses and trigger antiviral responses. Paradoxically, in the case of HIV-1, DCs might contribute to viral pathogenesis through trans-infection, a mechanism that promotes viral capture and transmission to target cells, especially after DC maturation. In this review, we highlight recent evidence identifying sialyllactose-containing gangliosides in the viral membrane and the cellular lectin Siglec-1 as critical determinants for HIV-1 capture and storage by mature DCs and for DC-mediated trans-infection of T cells. In contrast, DC-SIGN, long considered to be the main receptor for DC capture of HIV-1, plays a minor role in mature DC-mediated HIV-1 capture and trans-infection.

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          Taking dendritic cells into medicine.

          Ralph M. Steinman, Jacques Banchereau (2007)
          Dendritic cells (DCs) orchestrate a repertoire of immune responses that bring about resistance to infection and silencing or tolerance to self. In the settings of infection and cancer, microbes and tumours can exploit DCs to evade immunity, but DCs also can generate resistance, a capacity that is readily enhanced with DC-targeted vaccines. During allergy, autoimmunity and transplant rejection, DCs instigate unwanted responses that cause disease, but, again, DCs can be harnessed to silence these conditions with novel therapies. Here we present some medical implications of DC biology that account for illness and provide opportunities for prevention and therapy.
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            Indirect activation of naïve CD4+ T cells by dendritic cell-derived exosomes.

            Clotilde Théry, Livine Duban, Elodie Segura … (2002)
            Dendritic cells (DCs) secrete vesicles of endosomal origin, called exosomes, that bear major histocompatibility complex (MHC) and T cell costimulatory molecules. Here, we found that injection of antigen- or peptide-bearing exosomes induced antigen-specific naïve CD4+ T cell activation in vivo. In vitro, exosomes did not induce antigen-dependent T cell stimulation unless mature CD8alpha- DCs were also present in the cultures. These mature DCs could be MHC class II-negative, but had to bear CD80 and CD86. Therefore, in addition to carrying antigen, exosomes promote the exchange of functional peptide-MHC complexes between DCs. Such a mechanism may increase the number of DCs bearing a particular peptide, thus amplifying the initiation of primary adaptive immune responses.
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              Distribution and three-dimensional structure of AIDS virus envelope spikes.

              Ping Zhu, Jun Liu, Julian Bess … (2006)
              Envelope glycoprotein (Env) spikes on AIDS retroviruses initiate infection of host cells and are therefore targets for vaccine development. Though crystal structures for partial Env subunits are known, the structure and distribution of native Env spikes on virions is obscure. We applied cryoelectron microscopy tomography to define ultrastructural details of spikes. Virions of wild-type human immunodeficiency virus 1 (HIV-1) and a mutant simian immunodeficiency virus (SIV) had approximately 14 and approximately 73 spikes per particle, respectively, with some clustering of HIV-1 spikes. Three-dimensional averaging showed that the surface glycoprotein (gp120) 'head' of each subunit of the trimeric SIV spike contains a primary mass, with two secondary lobes. The transmembrane glycoprotein 'stalk' of each trimer is composed of three independent legs that project obliquely from the trimer head, tripod-like. Reconciling available atomic structures with the three-dimensional whole spike density map yields insights into the orientation of Env spike structural elements and possible structural bases of their functions.
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                Author and article information

                Contributors
                Tom C. Hobman: Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS Pathog
                Journal ID (iso-abbrev): PLoS Pathog
                Journal ID (publisher-id): plos
                Journal ID (pmc): plospath
                Title: PLoS Pathogens
                Publisher: Public Library of Science (San Francisco, USA )
                ISSN (Print): 1553-7366
                ISSN (Electronic): 1553-7374
                Publication date Collection: July 2014
                Publication date (Electronic): 17 July 2014
                Volume: 10
                Issue: 7
                Electronic Location Identifier: e1004146
                Affiliations
                [1 ]AIDS Research Institute IrsiCaixa, Institut d'Investigació en Ciències de la Salut Germans Trias i Pujol, Universitat Autònoma de Barcelona, Badalona, Spain
                [2 ]Unidad de Biofisica (CSIC-UPV/EHU) and Departamento de Bioquímica, Universidad del Pais Vasco, Bilbao, Spain
                [3 ]Institute of Microbiology, University Hospital Center and University of Lausanne, Lausanne, Switzerland
                [4 ]Department of Infectious Diseases, Virology, Universitätsklinikum Heidelberg, Heidelberg, Germany
                [5 ]Universitat de Vic–Universitat Central de Catalunya (UVic-UCC), Vic, Spain
                [6 ]Institució Catalana de Recerca i Estudis Avançats (ICREA), Barcelona, Spain
                University of Alberta, Canada
                Author notes

                The authors have declared that no competing interests exist.

                The authors have declared that no competing interests exist.

                ¶ These authors are joint senior authors on this work.

                Article
                Publisher ID: PPATHOGENS-D-14-00433
                DOI: 10.1371/journal.ppat.1004146
                PMC ID: 4102576
                PubMed ID: 25033082
                SO-VID: b43789d9-3e69-4add-aeaf-8c05b3edd267
                Copyright statement: Copyright @ 2014
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Page count
                Pages: 9
                Funding
                Work in JMP group is supported by the Spanish Ministry of Science and Innovation through grant SAF2010-21224 and the Spanish AIDS network “Red Temática Cooperativa de Investigación en SIDA” (RD06/0006). NIU is supported by the Mathilde Krim Fellowship in basic biomedical research 108676 founded by “AmfAR” AIDS research Foundation. The funders had no role in the design and preparation of this review, decision to publish, or preparation of the manuscript.
                Categories
                Subject: Review
                Subject: Biology and life sciences
                Subject: Immunology
                Subject: Clinical immunology
                Subject: HIV immunopathogenesis
                Subject: Microbiology
                Subject: Medical Microbiology
                Subject: Microbial Pathogens
                Subject: Viral Pathogens
                Subject: Immunodeficiency Viruses
                Subject: HIV
                Subject: Virology
                Subject: Viral Transmission and Infection
                Subject: Viral Attachment
                Subject: Viral Entry
                Subject: Viral Immune Evasion
                Subject: Medicine and Health Sciences
                Subject: Pathology and Laboratory Medicine
                Subject: Pathogenesis
                Subject: Host-Pathogen Interactions
                Subject: Pathogens
                Subject: Virulence Factors
                Subject: Infectious Diseases
                Subject: Viral Diseases

                ScienceOpen disciplines: Infectious disease & Microbiology
                Data availability:
                ScienceOpen disciplines: Infectious disease & Microbiology

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