MERS coronavirus nsp1 participates in an efficient propagation through a specific interaction with viral RNA.
Identifieur interne : 000B83 ( PubMed/Corpus ); précédent : 000B82; suivant : 000B84MERS coronavirus nsp1 participates in an efficient propagation through a specific interaction with viral RNA.
Auteurs : Yutaka Terada ; Kengo Kawachi ; Yoshiharu Matsuura ; Wataru KamitaniSource :
- Virology [ 1096-0341 ] ; 2017.
English descriptors
- KwdEn :
- Cell Line, DNA Mutational Analysis, Humans, Middle East Respiratory Syndrome Coronavirus (physiology), Mutant Proteins (genetics), Mutant Proteins (metabolism), RNA, Viral (metabolism), Reverse Genetics, Viral Nonstructural Proteins (genetics), Viral Nonstructural Proteins (metabolism), Virus Replication.
- MESH :
- chemical , genetics : Mutant Proteins, Viral Nonstructural Proteins.
- chemical , metabolism : Mutant Proteins, RNA, Viral, Viral Nonstructural Proteins.
- physiology : Middle East Respiratory Syndrome Coronavirus.
- Cell Line, DNA Mutational Analysis, Humans, Reverse Genetics, Virus Replication.
Abstract
MERS-CoV is the only lethal human CoV still endemic in the Arabian Peninsula and neither vaccine nor therapeutics against MERS-CoV infection is available. The nsp1 of CoV is thought to be a major virulence factor because it suppresses protein synthesis through the degradation of host mRNA. In contrast, viral RNA circumvents the nsp1-mediated translational shutoff for an efficient propagation. In this study, we identified amino acid residue in MERS-CoV nsp1 that differ from those of SARS-CoV nsp1, and that appear to be crucial for circumventing the translational shutoff. In addition, reverse genetics analysis suggested the presence of a cis-acting element at the 5'-terminus of the nsp1-coding region, which contributes to the specific recognition of viral RNA that is required for an efficient viral replication. Our results suggest the CoVs share a common mechanism for circumventing the nsp1-mediated translational shutoff.
DOI: 10.1016/j.virol.2017.08.026
PubMed: 28843094
Links to Exploration step
pubmed:28843094Le document en format XML
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Electronic address: wakamita@biken.osaka-u.ac.jp.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Virology</title><idno type="eISSN">1096-0341</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cell Line</term><term>DNA Mutational Analysis</term><term>Humans</term><term>Middle East Respiratory Syndrome Coronavirus (physiology)</term><term>Mutant Proteins (genetics)</term><term>Mutant Proteins (metabolism)</term><term>RNA, Viral (metabolism)</term><term>Reverse Genetics</term><term>Viral Nonstructural Proteins (genetics)</term><term>Viral Nonstructural Proteins (metabolism)</term><term>Virus Replication</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Mutant Proteins</term><term>Viral Nonstructural Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Mutant Proteins</term><term>RNA, Viral</term><term>Viral Nonstructural Proteins</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Middle East Respiratory Syndrome Coronavirus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line</term><term>DNA Mutational Analysis</term><term>Humans</term><term>Reverse Genetics</term><term>Virus Replication</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">MERS-CoV is the only lethal human CoV still endemic in the Arabian Peninsula and neither vaccine nor therapeutics against MERS-CoV infection is available. The nsp1 of CoV is thought to be a major virulence factor because it suppresses protein synthesis through the degradation of host mRNA. In contrast, viral RNA circumvents the nsp1-mediated translational shutoff for an efficient propagation. In this study, we identified amino acid residue in MERS-CoV nsp1 that differ from those of SARS-CoV nsp1, and that appear to be crucial for circumventing the translational shutoff. In addition, reverse genetics analysis suggested the presence of a cis-acting element at the 5'-terminus of the nsp1-coding region, which contributes to the specific recognition of viral RNA that is required for an efficient viral replication. Our results suggest the CoVs share a common mechanism for circumventing the nsp1-mediated translational shutoff.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28843094</PMID><DateCompleted><Year>2017</Year><Month>10</Month><Day>10</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>04</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1096-0341</ISSN><JournalIssue CitedMedium="Internet"><Volume>511</Volume><PubDate><Year>2017</Year><Month>11</Month></PubDate></JournalIssue><Title>Virology</Title><ISOAbbreviation>Virology</ISOAbbreviation></Journal><ArticleTitle>MERS coronavirus nsp1 participates in an efficient propagation through a specific interaction with viral RNA.</ArticleTitle><Pagination><MedlinePgn>95-105</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0042-6822(17)30289-1</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.virol.2017.08.026</ELocationID><Abstract><AbstractText>MERS-CoV is the only lethal human CoV still endemic in the Arabian Peninsula and neither vaccine nor therapeutics against MERS-CoV infection is available. The nsp1 of CoV is thought to be a major virulence factor because it suppresses protein synthesis through the degradation of host mRNA. In contrast, viral RNA circumvents the nsp1-mediated translational shutoff for an efficient propagation. In this study, we identified amino acid residue in MERS-CoV nsp1 that differ from those of SARS-CoV nsp1, and that appear to be crucial for circumventing the translational shutoff. In addition, reverse genetics analysis suggested the presence of a cis-acting element at the 5'-terminus of the nsp1-coding region, which contributes to the specific recognition of viral RNA that is required for an efficient viral replication. Our results suggest the CoVs share a common mechanism for circumventing the nsp1-mediated translational shutoff.</AbstractText><CopyrightInformation>Copyright © 2017 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Terada</LastName><ForeName>Yutaka</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Laboratory of Clinical Research on Infectious Diseases, Osaka University, Osaka 565-0871, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kawachi</LastName><ForeName>Kengo</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Laboratory of Clinical Research on Infectious Diseases, Osaka University, Osaka 565-0871, Japan; Department of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Matsuura</LastName><ForeName>Yoshiharu</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Molecular Virology, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kamitani</LastName><ForeName>Wataru</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Laboratory of Clinical Research on Infectious Diseases, Osaka University, Osaka 565-0871, Japan; Tsukuba Primate Research Center, National Institutes of Biomedical Innovation, Health and Nutrition, Tsukuba, Ibaraki 305-0843, Japan. 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