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      Flavivirus Cell Entry and Membrane Fusion

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          Abstract

          Flaviviruses, such as dengue virus and West Nile virus, are enveloped viruses that infect cells through receptor-mediated endocytosis and fusion from within acidic endosomes. The cell entry process of flaviviruses is mediated by the viral E glycoprotein. This short review will address recent advances in the understanding of flavivirus cell entry with specific emphasis on the recent study of Zaitseva and coworkers, indicating that anionic lipids might play a crucial role in the fusion process of dengue virus [ 1].

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          Composition and Three-Dimensional Architecture of the Dengue Virus Replication and Assembly Sites

          Sonja Welsch, Sven Miller, Inés Romero-Brey … (2009)
          Summary Positive-strand RNA viruses are known to rearrange cellular membranes to facilitate viral genome replication. The biogenesis and three-dimensional organization of these membranes and the link between replication and virus assembly sites is not fully clear. Using electron microscopy, we find Dengue virus (DENV)-induced vesicles, convoluted membranes, and virus particles to be endoplasmic reticulum (ER)-derived, and we detect double-stranded RNA, a presumed marker of RNA replication, inside virus-induced vesicles. Electron tomography (ET) shows DENV-induced membrane structures to be part of one ER-derived network. Furthermore, ET reveals vesicle pores that could enable release of newly synthesized viral RNA and reveals budding of DENV particles on ER membranes directly apposed to vesicle pores. Thus, DENV modifies ER membrane structure to promote replication and efficient encapsidation of the genome into progeny virus. This architecture of DENV replication and assembly sites could explain the coordination of distinct steps of the flavivirus replication cycle.
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            DC-SIGN (CD209) Mediates Dengue Virus Infection of Human Dendritic Cells

            Boonrat Tassaneetrithep, Timothy H. Burgess, Angela Granelli-Piperno … (2003)
            Dengue virus is a single-stranded, enveloped RNA virus that productively infects human dendritic cells (DCs) primarily at the immature stage of their differentiation. We now find that all four serotypes of dengue use DC-SIGN (CD209), a C-type lectin, to infect dendritic cells. THP-1 cells become susceptible to dengue infection after transfection of DC-specific ICAM-3 grabbing nonintegrin (DC-SIGN), or its homologue L-SIGN, whereas the infection of dendritic cells is blocked by anti–DC-SIGN antibodies and not by antibodies to other molecules on these cells. Viruses produced by dendritic cells are infectious for DC-SIGN– and L-SIGN–bearing THP-1 cells and other permissive cell lines. Therefore, DC-SIGN may be considered as a new target for designing therapies that block dengue infection.
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              CLEC5A is critical for dengue-virus-induced lethal disease.

              Kuo-Sheng Lee, Tzyy-Wen Chiou, Szu-Tah Chen … (2008)
              Dengue haemorrhagic fever and dengue shock syndrome, the most severe responses to dengue virus (DV) infection, are characterized by plasma leakage (due to increased vascular permeability) and low platelet counts. CLEC5A (C-type lectin domain family 5, member A; also known as myeloid DAP12-associating lectin (MDL-1)) contains a C-type lectin-like fold similar to the natural-killer T-cell C-type lectin domains and associates with a 12-kDa DNAX-activating protein (DAP12) on myeloid cells. Here we show that CLEC5A interacts with the dengue virion directly and thereby brings about DAP12 phosphorylation. The CLEC5A-DV interaction does not result in viral entry but stimulates the release of proinflammatory cytokines. Blockade of CLEC5A-DV interaction suppresses the secretion of proinflammatory cytokines without affecting the release of interferon-alpha, supporting the notion that CLEC5A acts as a signalling receptor for proinflammatory cytokine release. Moreover, anti-CLEC5A monoclonal antibodies inhibit DV-induced plasma leakage, as well as subcutaneous and vital-organ haemorrhaging, and reduce the mortality of DV infection by about 50% in STAT1-deficient mice. Our observation that blockade of CLEC5A-mediated signalling attenuates the production of proinflammatory cytokines by macrophages infected with DV (either alone or complexed with an enhancing antibody) offers a promising strategy for alleviating tissue damage and increasing the survival of patients suffering from dengue haemorrhagic fever and dengue shock syndrome, and possibly even other virus-induced inflammatory diseases.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Viruses
                Title: Viruses
                Publisher: Molecular Diversity Preservation International (MDPI)
                ISSN (Electronic): 1999-4915
                Publication date (Electronic): 22 February 2011
                Publication date Collection: February 2011
                Volume: 3
                Issue: 2
                Pages: 160-171
                Affiliations
                Department of Medical Microbiology, Molecular Virology Section, University Medical Center Groningen, University of Groningen, PO Box 30.001, 9700 RB Groningen, The Netherlands; E-Mails: b.j.s.moesker@ 123456med.umcg.nl (B.M.); i.a.rodenhuis-zybert@ 123456med.umcg.nl (I.R.-Z.); j.c.wilschut@ 123456med.umcg.nl (J.W.)
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: jolanda.smit@ 123456med.umcg.nl ; Tel.: +31-50-3632738; Fax: +31-50-3638171.
                Article
                Publisher ID: viruses-03-00160
                DOI: 10.3390/v3020160
                PMC ID: 3206597
                PubMed ID: 22049308
                SO-VID: b54ccc66-5548-4def-9300-3d7b131a47df
                Copyright © © 2011 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                Date received : 19 January 2011
                Date revision received : 10 February 2011
                Date accepted : 10 February 2011
                Categories
                Subject: Commentary

                ScienceOpen disciplines: Microbiology & Virology
                Keywords: dengue,negatively charged lipids,flavivirus,anionic lipids,west nile virus,membrane fusion,receptor,cell entry
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology
                Keywords: dengue, negatively charged lipids, flavivirus, anionic lipids, west nile virus, membrane fusion, receptor, cell entry

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