The role of programmed-1 ribosomal frameshifting in coronavirus propagation.
Identifieur interne : 001B30 ( PubMed/Curation ); précédent : 001B29; suivant : 001B31The role of programmed-1 ribosomal frameshifting in coronavirus propagation.
Auteurs : Ewan P. Plant [États-Unis] ; Jonathan D. DinmanSource :
- Frontiers in bioscience : a journal and virtual library [ 1093-9946 ] ; 2008.
Descripteurs français
- KwdFr :
- MESH :
- croissance et développement : Coronavirus.
- génétique : Coronavirus, Virus du SRAS.
- physiologie : Coronavirus, Virus du SRAS.
- virologie : Syndrome respiratoire aigu sévère.
- Cadres ouverts de lecture, Décalage ribosomique du cadre de lecture, Humains.
English descriptors
- KwdEn :
- MESH :
- genetics : Coronavirus, SARS Virus.
- growth & development : Coronavirus.
- physiology : Coronavirus, SARS Virus.
- virology : Severe Acute Respiratory Syndrome.
- Frameshifting, Ribosomal, Humans, Open Reading Frames.
Abstract
Coronaviruses have the potential to cause significant economic, agricultural and health problems. The severe acute respiratory syndrome (SARS) associated coronavirus outbreak in late 2002, early 2003 called attention to the potential damage that coronaviruses could cause in the human population. The ensuing research has enlightened many to the molecular biology of coronaviruses. A programmed -1 ribosomal frameshift is required by coronaviruses for the production of the RNA dependent RNA polymerase which in turn is essential for viral replication. The frameshifting signal encoded in the viral genome has additional features that are not essential for frameshifting. Elucidation of the differences between coronavirus frameshift signals and signals from other viruses may help our understanding of these features. Here we summarize current knowledge and add additional insight regarding the function of the programmed -1 ribosomal frameshift signal in the coronavirus lifecycle.
DOI: 10.2741/3046
PubMed: 18508552
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Plant</name><affiliation wicri:level="1"><nlm:affiliation>Division of Emerging and Transfusion Transmitted Diseases, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892, USA. Ewan.Plant@FDA.hhs.gov</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Emerging and Transfusion Transmitted Diseases, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892</wicri:regionArea></affiliation></author><author><name sortKey="Dinman, Jonathan D" sort="Dinman, Jonathan D" uniqKey="Dinman J" first="Jonathan D" last="Dinman">Jonathan D. Dinman</name></author></analytic><series><title level="j">Frontiers in bioscience : a journal and virtual library</title><idno type="ISSN">1093-9946</idno><imprint><date when="2008" type="published">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Coronavirus (genetics)</term><term>Coronavirus (growth & development)</term><term>Coronavirus (physiology)</term><term>Frameshifting, Ribosomal</term><term>Humans</term><term>Open Reading Frames</term><term>SARS Virus (genetics)</term><term>SARS Virus (physiology)</term><term>Severe Acute Respiratory Syndrome (virology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Cadres ouverts de lecture</term><term>Coronavirus (croissance et développement)</term><term>Coronavirus (génétique)</term><term>Coronavirus (physiologie)</term><term>Décalage ribosomique du cadre de lecture</term><term>Humains</term><term>Syndrome respiratoire aigu sévère (virologie)</term><term>Virus du SRAS (génétique)</term><term>Virus du SRAS (physiologie)</term></keywords><keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>Coronavirus</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Coronavirus</term><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Coronavirus</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Coronavirus</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Coronavirus</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Coronavirus</term><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Frameshifting, Ribosomal</term><term>Humans</term><term>Open Reading Frames</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Cadres ouverts de lecture</term><term>Décalage ribosomique du cadre de lecture</term><term>Humains</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Coronaviruses have the potential to cause significant economic, agricultural and health problems. The severe acute respiratory syndrome (SARS) associated coronavirus outbreak in late 2002, early 2003 called attention to the potential damage that coronaviruses could cause in the human population. The ensuing research has enlightened many to the molecular biology of coronaviruses. A programmed -1 ribosomal frameshift is required by coronaviruses for the production of the RNA dependent RNA polymerase which in turn is essential for viral replication. The frameshifting signal encoded in the viral genome has additional features that are not essential for frameshifting. Elucidation of the differences between coronavirus frameshift signals and signals from other viruses may help our understanding of these features. Here we summarize current knowledge and add additional insight regarding the function of the programmed -1 ribosomal frameshift signal in the coronavirus lifecycle.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">18508552</PMID><DateCompleted><Year>2008</Year><Month>09</Month><Day>19</Day></DateCompleted><DateRevised><Year>2019</Year><Month>09</Month><Day>02</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Print">1093-9946</ISSN><JournalIssue CitedMedium="Internet"><Volume>13</Volume><PubDate><Year>2008</Year><Month>May</Month><Day>01</Day></PubDate></JournalIssue><Title>Frontiers in bioscience : a journal and virtual library</Title><ISOAbbreviation>Front. Biosci.</ISOAbbreviation></Journal><ArticleTitle>The role of programmed-1 ribosomal frameshifting in coronavirus propagation.</ArticleTitle><Pagination><MedlinePgn>4873-81</MedlinePgn></Pagination><Abstract><AbstractText>Coronaviruses have the potential to cause significant economic, agricultural and health problems. The severe acute respiratory syndrome (SARS) associated coronavirus outbreak in late 2002, early 2003 called attention to the potential damage that coronaviruses could cause in the human population. The ensuing research has enlightened many to the molecular biology of coronaviruses. A programmed -1 ribosomal frameshift is required by coronaviruses for the production of the RNA dependent RNA polymerase which in turn is essential for viral replication. The frameshifting signal encoded in the viral genome has additional features that are not essential for frameshifting. Elucidation of the differences between coronavirus frameshift signals and signals from other viruses may help our understanding of these features. Here we summarize current knowledge and add additional insight regarding the function of the programmed -1 ribosomal frameshift signal in the coronavirus lifecycle.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Plant</LastName><ForeName>Ewan P</ForeName><Initials>EP</Initials><AffiliationInfo><Affiliation>Division of Emerging and Transfusion Transmitted Diseases, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892, USA. 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