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      CRISPR-Cas Targeting of Host Genes as an Antiviral Strategy

      review-article
      Author(s): 1 , 2 , 3 , *
      Publication date (Electronic):
      Journal: Viruses
      Publisher: MDPI
      Keywords: gene targeting, CRISPR-Cas, host genes, virus, antiviral strategy

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          Abstract

          Currently, a new gene editing tool—the Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) associated (Cas) system—is becoming a promising approach for genetic manipulation at the genomic level. This simple method, originating from the adaptive immune defense system in prokaryotes, has been developed and applied to antiviral research in humans. Based on the characteristics of virus-host interactions and the basic rules of nucleic acid cleavage or gene activation of the CRISPR-Cas system, it can be used to target both the virus genome and host factors to clear viral reservoirs and prohibit virus infection or replication. Here, we summarize recent progress of the CRISPR-Cas technology in editing host genes as an antiviral strategy.

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          Characterization of a novel coronavirus associated with severe acute respiratory syndrome.

          P Rota (2003)
          In March 2003, a novel coronavirus (SARS-CoV) was discovered in association with cases of severe acute respiratory syndrome (SARS). The sequence of the complete genome of SARS-CoV was determined, and the initial characterization of the viral genome is presented in this report. The genome of SARS-CoV is 29,727 nucleotides in length and has 11 open reading frames, and its genome organization is similar to that of other coronaviruses. Phylogenetic analyses and sequence comparisons showed that SARS-CoV is not closely related to any of the previously characterized coronaviruses.
          Article 0 comments Cited 1235 times – based on 0 reviews     Review now
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            Sodium taurocholate cotransporting polypeptide is a functional receptor for human hepatitis B and D virus

            Huan Yan, Guocai Zhong, Guangwei Xu … (2012)
            Human hepatitis B virus (HBV) infection and HBV-related diseases remain a major public health problem. Individuals coinfected with its satellite hepatitis D virus (HDV) have more severe disease. Cellular entry of both viruses is mediated by HBV envelope proteins. The pre-S1 domain of the large envelope protein is a key determinant for receptor(s) binding. However, the identity of the receptor(s) is unknown. Here, by using near zero distance photo-cross-linking and tandem affinity purification, we revealed that the receptor-binding region of pre-S1 specifically interacts with sodium taurocholate cotransporting polypeptide (NTCP), a multiple transmembrane transporter predominantly expressed in the liver. Silencing NTCP inhibited HBV and HDV infection, while exogenous NTCP expression rendered nonsusceptible hepatocarcinoma cells susceptible to these viral infections. Moreover, replacing amino acids 157–165 of nonfunctional monkey NTCP with the human counterpart conferred its ability in supporting both viral infections. Our results demonstrate that NTCP is a functional receptor for HBV and HDV. DOI: http://dx.doi.org/10.7554/eLife.00049.001
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              Tetherin inhibits retrovirus release and is antagonized by HIV-1 Vpu.

              Stuart J D Neil, Trinity Zang, Paul D. Bieniasz (2008)
              Human cells possess an antiviral activity that inhibits the release of retrovirus particles, and other enveloped virus particles, and is antagonized by the HIV-1 accessory protein, Vpu. This antiviral activity can be constitutively expressed or induced by interferon-alpha, and it consists of protein-based tethers, which we term 'tetherins', that cause retention of fully formed virions on infected cell surfaces. Using deductive constraints and gene expression analyses, we identify CD317 (also called BST2 or HM1.24), a membrane protein of previously unknown function, as a tetherin. Specifically, CD317 expression correlated with, and induced, a requirement for Vpu during HIV-1 and murine leukaemia virus particle release. Furthermore, in cells where HIV-1 virion release requires Vpu expression, depletion of CD317 abolished this requirement. CD317 caused retention of virions on cell surfaces and, after endocytosis, in CD317-positive compartments. Vpu co-localized with CD317 and inhibited these effects. Inhibition of Vpu function and consequent mobilization of tetherin's antiviral activity is a potential therapeutic strategy in HIV/AIDS.
              Article 0 comments Cited 687 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Viruses
                Journal ID (iso-abbrev): Viruses
                Journal ID (publisher-id): viruses
                Title: Viruses
                Publisher: MDPI
                ISSN (Electronic): 1999-4915
                Publication date (Electronic): 16 January 2018
                Publication date Collection: January 2018
                Volume: 10
                Issue: 1
                Electronic Location Identifier: 40
                Affiliations
                [1 ]School of Basic Medical Sciences, Wuhan University, Wuhan 430071, China; Chen-shuliang@ 123456whu.edu.cn
                [2 ]Institute of Health Inspection and Testing, Hubei Provincial Center for Disease Control and Prevention, Wuhan 430079, China; fish-yuxiao@ 123456hotmail.com
                [3 ]School of Medicine (Shenzhen), Sun Yat-sen University, Guangzhou 510080, China
                Author notes
                [* ]Correspondence: guodeyin@ 123456mail.sysu.edu.cn ; Tel./Fax: +86-20-8733-5130
                Article
                Publisher ID: viruses-10-00040
                DOI: 10.3390/v10010040
                PMC ID: 5795453
                PubMed ID: 29337866
                SO-VID: 604908a9-5549-4fef-8709-596597c422bc
                Copyright © © 2018 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 24 December 2017
                Date accepted : 14 January 2018
                Categories
                Subject: Review

                ScienceOpen disciplines: Microbiology & Virology
                Keywords: gene targeting,crispr-cas,host genes,virus,antiviral strategy
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology
                Keywords: gene targeting, crispr-cas, host genes, virus, antiviral strategy

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