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      Human Coronaviruses: A Review of Virus–Host Interactions

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          Abstract

          Human coronaviruses (HCoVs) are known respiratory pathogens associated with a range of respiratory outcomes. In the past 14 years, the onset of severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) have thrust HCoVs into spotlight of the research community due to their high pathogenicity in humans. The study of HCoV-host interactions has contributed extensively to our understanding of HCoV pathogenesis. In this review, we discuss some of the recent findings of host cell factors that might be exploited by HCoVs to facilitate their own replication cycle. We also discuss various cellular processes, such as apoptosis, innate immunity, ER stress response, mitogen-activated protein kinase (MAPK) pathway and nuclear factor kappa B (NF-κB) pathway that may be modulated by HCoVs.

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          Angiotensin-converting enzyme 2 is a functional receptor for the SARS coronavirus

          Wenhui Li, Michael Moore, Natalya Vasilieva … (2003)
          Spike (S) proteins of coronaviruses, including the coronavirus that causes severe acute respiratory syndrome (SARS), associate with cellular receptors to mediate infection of their target cells 1,2 . Here we identify a metallopeptidase, angiotensin-converting enzyme 2 (ACE2) 3,4 , isolated from SARS coronavirus (SARS-CoV)-permissive Vero E6 cells, that efficiently binds the S1 domain of the SARS-CoV S protein. We found that a soluble form of ACE2, but not of the related enzyme ACE1, blocked association of the S1 domain with Vero E6 cells. 293T cells transfected with ACE2, but not those transfected with human immunodeficiency virus-1 receptors, formed multinucleated syncytia with cells expressing S protein. Furthermore, SARS-CoV replicated efficiently on ACE2-transfected but not mock-transfected 293T cells. Finally, anti-ACE2 but not anti-ACE1 antibody blocked viral replication on Vero E6 cells. Together our data indicate that ACE2 is a functional receptor for SARS-CoV. Supplementary information The online version of this article (doi:10.1038/nature02145) contains supplementary material, which is available to authorized users.
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            Regulation of type I interferon responses.

            Lionel B Ivashkiv, Laura Donlin (2014)
            Type I interferons (IFNs) activate intracellular antimicrobial programmes and influence the development of innate and adaptive immune responses. Canonical type I IFN signalling activates the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway, leading to transcription of IFN-stimulated genes (ISGs). Host, pathogen and environmental factors regulate the responses of cells to this signalling pathway and thus calibrate host defences while limiting tissue damage and preventing autoimmunity. Here, we summarize the signalling and epigenetic mechanisms that regulate type I IFN-induced STAT activation and ISG transcription and translation. These regulatory mechanisms determine the biological outcomes of type I IFN responses and whether pathogens are cleared effectively or chronic infection or autoimmune disease ensues.
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              Inflammasomes: mechanism of action, role in disease, and therapeutics.

              Haitao Guo, Justin Callaway, Jenny P.-Y. Ting (2015)
              The inflammasomes are innate immune system receptors and sensors that regulate the activation of caspase-1 and induce inflammation in response to infectious microbes and molecules derived from host proteins. They have been implicated in a host of inflammatory disorders. Recent developments have greatly enhanced our understanding of the molecular mechanisms by which different inflammasomes are activated. Additionally, increasing evidence in mouse models, supported by human data, strongly implicates an involvement of the inflammasome in the initiation or progression of diseases with a high impact on public health, such as metabolic disorders and neurodegenerative diseases. Finally, recent developments pointing toward promising therapeutics that target inflammasome activity in inflammatory diseases have been reported. This review will focus on these three areas of inflammasome research.
              Article 0 comments Cited 755 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Maurizio Battino: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): Diseases
                Journal ID (iso-abbrev): Diseases
                Journal ID (publisher-id): diseases
                Title: Diseases
                Publisher: MDPI
                ISSN (Electronic): 2079-9721
                Publication date (Electronic): 25 July 2016
                Publication date Collection: September 2016
                Volume: 4
                Issue: 3
                Electronic Location Identifier: 26
                Affiliations
                School of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, Singapore 637551, Singapore; YVON0016@ 123456e.ntu.edu.sg (Y.X.L.); S150004@ 123456e.ntu.edu.sg (Y.L.N.); JPTAM@ 123456ntu.edu.sg (J.P.T.)
                Author notes
                [* ]Correspondence: dxliu0001@ 123456163.com ; Tel.: +65-6316-2861
                Article
                Publisher ID: diseases-04-00026
                DOI: 10.3390/diseases4030026
                PMC ID: 5456285
                PubMed ID: 28933406
                SO-VID: ef8d4fd5-8335-4969-a43b-d26d536d19eb
                Copyright © © 2016 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 : 08 June 2016
                Date accepted : 18 July 2016
                Categories
                Subject: Review

                Keywords: human coronavirus,virus–host interactions,apoptosis,innate immunity,er stress,mapk,nf-κb
                Data availability:
                Keywords: human coronavirus, virus–host interactions, apoptosis, innate immunity, er stress, mapk, nf-κb

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