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Coronavirus Genome Structure and Replication

Identifieur interne : 000147 ( Pmc/Curation ); précédent : 000146; suivant : 000148

Coronavirus Genome Structure and Replication

Auteurs :

Source :

RBID : PMC:7120446

Abstract

In addition to the SARS coronavirus (treated separately elsewhere in this volume), the complete genome sequences of six species in the coronavirus genus of the coronavirus family [avian infectious bronchitis virus-Beaudette strain (IBV-Beaudette), bovine coronavirus-ENT strain (BCoV-ENT), human coronavirus-229E strain (HCoV-229E), murine hepatitis virus-A59 strain (MHV-A59), porcine transmissible gastroenteritis-Purdue 115 strain (TGEV-Purdue 115), and porcine epidemic diarrhea virus-CV777 strain (PEDV-CV777)] have now been reported. Their lengths range from 27,317 nt for HCoV-229E to 31,357 nt for the murine hepatitis virus-A59, establishing the coronavirus genome as the largest known among RNA viruses. The basic organization of the coronavirus genome is shared with other members of the Nidovirus order (the torovirus genus, also in the family Coronaviridae, and members of the family Arteriviridae) in that the nonstructural proteins involved in proteolytic processing, genome replication, and subgenomic mRNA synthesis (transcription) (an estimated 14–16 end products for coronaviruses) are encoded within the 5′-proximal two-thirds of the genome on gene 1 and the (mostly) structural proteins are encoded within the 3′-proximal one-third of the genome (8–9 genes for coronaviruses). Genes for the major structural proteins in all coronaviruses occur in the 5′ to 3′ order as S, E, M, and N. The precise strategy used by coronaviruses for genome replication is not yet known, but many features have been established. This chapter focuses on some of the known features and presents some current questions regarding genome replication strategy, the cis-acting elements necessary for genome replication [as inferred from defective interfering (DI) RNA molecules], the minimum sequence requirements for autonomous replication of an RNA replicon, and the importance of gene order in genome replication.


Url:
DOI: 10.1007/3-540-26765-4_1
PubMed: 15609507
PubMed Central: 7120446

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PMC:7120446

Le document en format XML

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<p>In addition to the SARS coronavirus (treated separately elsewhere in this volume), the complete genome sequences of six species in the coronavirus genus of the coronavirus family [avian infectious bronchitis virus-Beaudette strain (IBV-Beaudette), bovine coronavirus-ENT strain (BCoV-ENT), human coronavirus-229E strain (HCoV-229E), murine hepatitis virus-A59 strain (MHV-A59), porcine transmissible gastroenteritis-Purdue 115 strain (TGEV-Purdue 115), and porcine epidemic diarrhea virus-CV777 strain (PEDV-CV777)] have now been reported. Their lengths range from 27,317 nt for HCoV-229E to 31,357 nt for the murine hepatitis virus-A59, establishing the coronavirus genome as the largest known among RNA viruses. The basic organization of the coronavirus genome is shared with other members of the Nidovirus order (the torovirus genus, also in the family
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) in that the nonstructural proteins involved in proteolytic processing, genome replication, and subgenomic mRNA synthesis (transcription) (an estimated 14–16 end products for coronaviruses) are encoded within the 5′-proximal two-thirds of the genome on gene 1 and the (mostly) structural proteins are encoded within the 3′-proximal one-third of the genome (8–9 genes for coronaviruses). Genes for the major structural proteins in all coronaviruses occur in the 5′ to 3′ order as S, E, M, and N. The precise strategy used by coronaviruses for genome replication is not yet known, but many features have been established. This chapter focuses on some of the known features and presents some current questions regarding genome replication strategy, the
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<name sortKey="Shaw, K" uniqKey="Shaw K">K. Shaw</name>
</author>
<author>
<name sortKey="Cavanagh, D" uniqKey="Cavanagh D">D. Cavanagh</name>
</author>
</analytic>
</biblStruct>
<biblStruct>
<analytic>
<author>
<name sortKey="Ziebuhr, J" uniqKey="Ziebuhr J">J. Ziebuhr</name>
</author>
<author>
<name sortKey="Snijder, E J" uniqKey="Snijder E">E.J. Snijder</name>
</author>
<author>
<name sortKey="Gorbalenya, A E" uniqKey="Gorbalenya A">A.E. Gorbalenya</name>
</author>
</analytic>
</biblStruct>
</listBibl>
</div1>
</back>
</TEI>
<pmc article-type="chapter-article">
<pmc-dir>properties open_access</pmc-dir>
<front>
<journal-meta>
<journal-id journal-id-type="publisher-id">978-3-540-26765-2</journal-id>
<journal-id journal-id-type="doi">10.1007/b138038</journal-id>
<journal-id journal-id-type="nlm-ta">Coronavirus Replication and Reverse Genetics</journal-id>
<journal-title-group>
<journal-title>Coronavirus Replication and Reverse Genetics</journal-title>
</journal-title-group>
<isbn publication-format="print">978-3-540-21494-6</isbn>
<isbn publication-format="electronic">978-3-540-26765-2</isbn>
</journal-meta>
<article-meta>
<article-id pub-id-type="pmid">15609507</article-id>
<article-id pub-id-type="pmc">7120446</article-id>
<article-id pub-id-type="publisher-id">1</article-id>
<article-id pub-id-type="doi">10.1007/3-540-26765-4_1</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Article</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Coronavirus Genome Structure and Replication</article-title>
</title-group>
<contrib-group content-type="book editors">
<contrib contrib-type="editor">
<name>
<surname>Enjuanes</surname>
<given-names>Luis</given-names>
</name>
<address>
<email>L.Enjuanes@cnb.uam.es</email>
</address>
<xref ref-type="aff" rid="Aff10"></xref>
</contrib>
<aff id="Aff10">
<institution-wrap>
<institution-id institution-id-type="GRID">grid.428469.5</institution-id>
<institution-id institution-id-type="ISNI">0000000417941018</institution-id>
<institution>Department of Molecular and Cell Biology,</institution>
<institution>Centro Nacional de Biotecnología,</institution>
</institution-wrap>
Campus Universidad Autónoma, Cantoblanco, 38049 Madrid, Spain</aff>
</contrib-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Brian</surname>
<given-names>D. A.</given-names>
</name>
<address>
<email>dbrian@utk.edu</email>
</address>
<xref ref-type="aff" rid="Aff11">11</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Baric</surname>
<given-names>R. S.</given-names>
</name>
<xref ref-type="aff" rid="Aff12">12</xref>
<xref ref-type="aff" rid="Aff13">13</xref>
</contrib>
<aff id="Aff11">
<label>11</label>
<institution-wrap>
<institution-id institution-id-type="GRID">grid.411461.7</institution-id>
<institution-id institution-id-type="ISNI">0000000123151184</institution-id>
<institution>Departments of Microbiology and Pathobiology,</institution>
<institution>University of Tennessee, College of Veterinary Medicine,</institution>
</institution-wrap>
Knoxville, TN 37996-0845 USA</aff>
<aff id="Aff12">
<label>12</label>
<institution-wrap>
<institution-id institution-id-type="GRID">grid.10698.36</institution-id>
<institution-id institution-id-type="ISNI">0000000122483208</institution-id>
<institution>Department of Microbiology and Immunology, School of Medicine,</institution>
<institution>University of North Carolina,</institution>
</institution-wrap>
Chapel Hill, NV 27599-7400 USA</aff>
<aff id="Aff13">
<label>13</label>
<institution-wrap>
<institution-id institution-id-type="GRID">grid.10698.36</institution-id>
<institution-id institution-id-type="ISNI">0000000122483208</institution-id>
<institution>Department of Epidemiology, Program of Infectious Diseases, School of Public Health,</institution>
<institution>University of North Carolina,</institution>
</institution-wrap>
Chapel Hill, NC 27599-7400 USA</aff>
</contrib-group>
<pub-date pub-type="ppub">
<year>2005</year>
</pub-date>
<volume>287</volume>
<fpage>1</fpage>
<lpage>30</lpage>
<permissions>
<copyright-statement>© Springer-Verlag 2005</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">
<p>In addition to the SARS coronavirus (treated separately elsewhere in this volume), the complete genome sequences of six species in the coronavirus genus of the coronavirus family [avian infectious bronchitis virus-Beaudette strain (IBV-Beaudette), bovine coronavirus-ENT strain (BCoV-ENT), human coronavirus-229E strain (HCoV-229E), murine hepatitis virus-A59 strain (MHV-A59), porcine transmissible gastroenteritis-Purdue 115 strain (TGEV-Purdue 115), and porcine epidemic diarrhea virus-CV777 strain (PEDV-CV777)] have now been reported. Their lengths range from 27,317 nt for HCoV-229E to 31,357 nt for the murine hepatitis virus-A59, establishing the coronavirus genome as the largest known among RNA viruses. The basic organization of the coronavirus genome is shared with other members of the Nidovirus order (the torovirus genus, also in the family
<italic>Coronaviridae</italic>
, and members of the family
<italic>Arteriviridae</italic>
) in that the nonstructural proteins involved in proteolytic processing, genome replication, and subgenomic mRNA synthesis (transcription) (an estimated 14–16 end products for coronaviruses) are encoded within the 5′-proximal two-thirds of the genome on gene 1 and the (mostly) structural proteins are encoded within the 3′-proximal one-third of the genome (8–9 genes for coronaviruses). Genes for the major structural proteins in all coronaviruses occur in the 5′ to 3′ order as S, E, M, and N. The precise strategy used by coronaviruses for genome replication is not yet known, but many features have been established. This chapter focuses on some of the known features and presents some current questions regarding genome replication strategy, the
<italic>cis</italic>
-acting elements necessary for genome replication [as inferred from defective interfering (DI) RNA molecules], the minimum sequence requirements for autonomous replication of an RNA replicon, and the importance of gene order in genome replication.</p>
</abstract>
<kwd-group xml:lang="en">
<title>Keywords</title>
<kwd>Infectious Bronchitis Virus</kwd>
<kwd>Genome Replication</kwd>
<kwd>Mouse Hepatitis Virus</kwd>
<kwd>Murine Coronavirus</kwd>
<kwd>Slippery Sequence</kwd>
</kwd-group>
<custom-meta-group>
<custom-meta>
<meta-name>issue-copyright-statement</meta-name>
<meta-value>© Springer-Verlag Berlin Heidelberg 2005</meta-value>
</custom-meta>
</custom-meta-group>
</article-meta>
</front>
</pmc>
</record>

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