Coronaviruses post-SARS: update on replication and pathogenesis
Identifieur interne : 000567 ( Pmc/Curation ); précédent : 000566; suivant : 000568Coronaviruses post-SARS: update on replication and pathogenesis
Auteurs : Stanley Perlman ; Jason NetlandSource :
- Nature Reviews. Microbiology [ 1740-1526 ] ; 2009.
Abstract
Coronaviruses are positive strand RNA viruses that cause disease in humans, and domestic and companion animals. They are most notorious for causing severe acute respiratory syndrome (SARS) outbreaks in 2002–2003. All coronaviruses follow the same basic strategy of replication. All coronaviruses encode 15 or 16 replicase related proteins, 4 or 5 structural proteins and 1–8 group-specific or accessory proteins. Many of the replicase proteins are assembled into replication machinery in double-membrane vesicles (DMVs) and on a reticular network of membranes that are derived from the endoplasmic reticulum. Coronaviruses are readily transmitted across species. This phenomenon was illustrated when the SARS-coronavirus crossed species from bats to intermediate hosts, such as palm civets, and then to humans. It also explains the large number of species, including humans, that are infected with viruses closely related to bovine coronavirus. In many coronavirus infections, disease severity increases during virus clearance, suggesting that the host immune response is both protective and pathogenic. Furthermore, inhibition of specific aspects of the immune response results in less severe disease and less tissue destruction, without diminishing the kinetics of virus clearance. Like all successful viruses, coronaviruses have evolved both passive and active mechanisms to evade the interferon response. Replication in DMVs may contribute to passive evasion of the innate immune response by making double-stranded RNA inaccessible to cellular sensors.
Url:
DOI: 10.1038/nrmicro2147
PubMed: 19430490
PubMed Central: 2830095
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Coronaviruses post-SARS: update on replication and pathogenesis</title><author><name sortKey="Perlman, Stanley" sort="Perlman, Stanley" uniqKey="Perlman S" first="Stanley" last="Perlman">Stanley Perlman</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Netland, Jason" sort="Netland, Jason" uniqKey="Netland J" first="Jason" last="Netland">Jason Netland</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">19430490</idno><idno type="pmc">2830095</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2830095</idno><idno type="RBID">PMC:2830095</idno><idno type="doi">10.1038/nrmicro2147</idno><date when="2009">2009</date><idno type="wicri:Area/Pmc/Corpus">000567</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000567</idno><idno type="wicri:Area/Pmc/Curation">000567</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000567</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Coronaviruses post-SARS: update on replication and pathogenesis</title><author><name sortKey="Perlman, Stanley" sort="Perlman, Stanley" uniqKey="Perlman S" first="Stanley" last="Perlman">Stanley Perlman</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author><author><name sortKey="Netland, Jason" sort="Netland, Jason" uniqKey="Netland J" first="Jason" last="Netland">Jason Netland</name><affiliation><nlm:aff id="Aff1"></nlm:aff></affiliation></author></analytic><series><title level="j">Nature Reviews. Microbiology</title><idno type="ISSN">1740-1526</idno><idno type="eISSN">1740-1534</idno><imprint><date when="2009">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><title>Key Points</title><p id="Par3"><list list-type="bullet"><list-item><p id="Par4">Coronaviruses are positive strand RNA viruses that cause disease in humans, and domestic and companion animals. They are most notorious for causing severe acute respiratory syndrome (SARS) outbreaks in 2002–2003. All coronaviruses follow the same basic strategy of replication.</p></list-item><list-item><p id="Par5">All coronaviruses encode 15 or 16 replicase related proteins, 4 or 5 structural proteins and 1–8 group-specific or accessory proteins. Many of the replicase proteins are assembled into replication machinery in double-membrane vesicles (DMVs) and on a reticular network of membranes that are derived from the endoplasmic reticulum.</p></list-item><list-item><p id="Par6">Coronaviruses are readily transmitted across species. This phenomenon was illustrated when the SARS-coronavirus crossed species from bats to intermediate hosts, such as palm civets, and then to humans. It also explains the large number of species, including humans, that are infected with viruses closely related to bovine coronavirus.</p></list-item><list-item><p id="Par7">In many coronavirus infections, disease severity increases during virus clearance, suggesting that the host immune response is both protective and pathogenic. Furthermore, inhibition of specific aspects of the immune response results in less severe disease and less tissue destruction, without diminishing the kinetics of virus clearance.</p></list-item><list-item><p id="Par8">Like all successful viruses, coronaviruses have evolved both passive and active mechanisms to evade the interferon response. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Nat Rev Microbiol</journal-id><journal-id journal-id-type="iso-abbrev">Nat. Rev. Microbiol</journal-id><journal-title-group><journal-title>Nature Reviews. Microbiology</journal-title></journal-title-group><issn pub-type="ppub">1740-1526</issn><issn pub-type="epub">1740-1534</issn><publisher><publisher-name>Nature Publishing Group UK</publisher-name><publisher-loc>London</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">19430490</article-id><article-id pub-id-type="pmc">2830095</article-id><article-id pub-id-type="publisher-id">BFnrmicro2147</article-id><article-id pub-id-type="doi">10.1038/nrmicro2147</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Coronaviruses post-SARS: update on replication and pathogenesis</article-title></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name><surname>Perlman</surname><given-names>Stanley</given-names></name><address><email>stanley-perlman@uiowa.edu</email></address><xref ref-type="aff" rid="Aff1"></xref><bio><p id="Par1">Stanley Perlman is a professor of microbiology and of paediatrics at the University of Iowa, USA. He received a Ph.D. in biophysics from the Massachusetts Institute of Technology, USA, and an M.D. from the University of Miami, USA. After completing clinical training in paediatrics and infectious diseases, he began studies of the pathogenesis of neurotropic strains of murine coronaviruses. His current work continues these studies and also uses molecular virology and mouse models to probe the host response to the severe acute respirator syndrome (SARS)-coronavirus.</p></bio></contrib><contrib contrib-type="author"><name><surname>Netland</surname><given-names>Jason</given-names></name><xref ref-type="aff" rid="Aff1"></xref><bio><p id="Par2">Jason Netland received his Ph.D. in immunology from the University of Iowa and is now pursuing postdoctoral work at the University of Washington, USA. His Ph.D. thesis entailed studies of SARS-coronavirus replication in mice. His interests are in the immune response to viral pathogens.</p></bio></contrib><aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.214572.7</institution-id><institution-id institution-id-type="ISNI">0000 0004 1936 8294</institution-id><institution>Department of Microbiology and Interdisciplinary Program in Immunology,</institution><institution>University of Iowa,</institution></institution-wrap>Iowa City, 52242 Iowa USA</aff></contrib-group><pub-date pub-type="epub"><day>11</day><month>5</month><year>2009</year></pub-date><pub-date pub-type="ppub"><year>2009</year></pub-date><volume>7</volume><issue>6</issue><fpage>439</fpage><lpage>450</lpage><permissions><copyright-statement>© Nature Publishing Group 2009</copyright-statement><license><license-p>This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.</license-p></license></permissions><abstract id="Abs1" abstract-type="KeyPoints"><title>Key Points</title><p id="Par3"><list list-type="bullet"><list-item><p id="Par4">Coronaviruses are positive strand RNA viruses that cause disease in humans, and domestic and companion animals. They are most notorious for causing severe acute respiratory syndrome (SARS) outbreaks in 2002–2003. All coronaviruses follow the same basic strategy of replication.</p></list-item><list-item><p id="Par5">All coronaviruses encode 15 or 16 replicase related proteins, 4 or 5 structural proteins and 1–8 group-specific or accessory proteins. Many of the replicase proteins are assembled into replication machinery in double-membrane vesicles (DMVs) and on a reticular network of membranes that are derived from the endoplasmic reticulum.</p></list-item><list-item><p id="Par6">Coronaviruses are readily transmitted across species. This phenomenon was illustrated when the SARS-coronavirus crossed species from bats to intermediate hosts, such as palm civets, and then to humans. It also explains the large number of species, including humans, that are infected with viruses closely related to bovine coronavirus.</p></list-item><list-item><p id="Par7">In many coronavirus infections, disease severity increases during virus clearance, suggesting that the host immune response is both protective and pathogenic. Furthermore, inhibition of specific aspects of the immune response results in less severe disease and less tissue destruction, without diminishing the kinetics of virus clearance.</p></list-item><list-item><p id="Par8">Like all successful viruses, coronaviruses have evolved both passive and active mechanisms to evade the interferon response. Replication in DMVs may contribute to passive evasion of the innate immune response by making double-stranded RNA inaccessible to cellular sensors.</p></list-item></list></p></abstract><abstract id="Abs2" abstract-type="web-summary"><p id="Par9">Coronaviruses gained prominence during the SARS outbreaks of 2002–2003, but there are many different coronaviruses that infect humans and animals. Perlman and Netland describe the biology of the coronaviruses, including their replication, host immune response and interspecies transmission.</p></abstract><abstract id="Abs3"><p id="Par10">Although coronaviruses were first identified nearly 60 years ago, they only received notoriety in 2003 when one of their members was identified as the aetiological agent of severe acute respiratory syndrome. Previously these viruses were known to be important agents of respiratory and enteric infections of domestic and companion animals and to cause approximately 15% of all cases of the common cold. This Review focuses on recent advances in our understanding of the mechanisms of coronavirus replication, interactions with the host immune response and disease pathogenesis. It also highlights the recent identification of numerous novel coronaviruses and the propensity of this virus family to cross species barriers.</p></abstract><custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name><meta-value>© Springer Nature Limited 2009</meta-value></custom-meta></custom-meta-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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