A live, impaired-fidelity coronavirus vaccine protects in an aged, immunocompromised mouse model of lethal disease.
Identifieur interne : 001288 ( PubMed/Curation ); précédent : 001287; suivant : 001289A live, impaired-fidelity coronavirus vaccine protects in an aged, immunocompromised mouse model of lethal disease.
Auteurs : Rachel L. Graham [États-Unis] ; Michelle M. Becker ; Lance D. Eckerle ; Meagan Bolles ; Mark R. Denison ; Ralph S. BaricSource :
- Nature medicine [ 1546-170X ] ; 2012.
Descripteurs français
- KwdFr :
- Amorces ADN (génétique), Analyse de séquence d'ADN, Animaux, Conception de médicament, Données de séquences moléculaires, Exoribonucleases (antagonistes et inhibiteurs), Exoribonucleases (génétique), Exoribonucleases (métabolisme), Exoribonucleases (physiologie), Facteurs de l'âge, Femelle, Plasmides (génétique), Réaction de polymérisation en chaine en temps réel, Réplication virale (physiologie), Souris, Souris de lignée BALB C, Statistique non paramétrique, Sujet immunodéprimé (immunologie), Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (traitement médicamenteux), Syndrome respiratoire aigu sévère (virologie), Séquence nucléotidique, Vaccins antiviraux (pharmacologie), Virus du SRAS (enzymologie), Virus du SRAS (génétique), Virus du SRAS (pathogénicité).
- MESH :
- antagonistes et inhibiteurs : Exoribonucleases.
- enzymologie : Virus du SRAS.
- génétique : Amorces ADN, Exoribonucleases, Plasmides, Virus du SRAS.
- immunologie : Sujet immunodéprimé, Syndrome respiratoire aigu sévère.
- métabolisme : Exoribonucleases.
- pathogénicité : Virus du SRAS.
- pharmacologie : Vaccins antiviraux.
- physiologie : Exoribonucleases, Réplication virale.
- traitement médicamenteux : Syndrome respiratoire aigu sévère.
- virologie : Syndrome respiratoire aigu sévère.
- Analyse de séquence d'ADN, Animaux, Conception de médicament, Données de séquences moléculaires, Facteurs de l'âge, Femelle, Réaction de polymérisation en chaine en temps réel, Souris, Souris de lignée BALB C, Statistique non paramétrique, Séquence nucléotidique.
English descriptors
- KwdEn :
- Age Factors, Animals, Base Sequence, DNA Primers (genetics), Drug Design, Exoribonucleases (antagonists & inhibitors), Exoribonucleases (genetics), Exoribonucleases (metabolism), Exoribonucleases (physiology), Female, Immunocompromised Host (immunology), Mice, Mice, Inbred BALB C, Molecular Sequence Data, Plasmids (genetics), Real-Time Polymerase Chain Reaction, SARS Virus (enzymology), SARS Virus (genetics), SARS Virus (pathogenicity), Sequence Analysis, DNA, Severe Acute Respiratory Syndrome (drug therapy), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (virology), Statistics, Nonparametric, Viral Vaccines (pharmacology), Virus Replication (physiology).
- MESH :
- chemical , antagonists & inhibitors : Exoribonucleases.
- chemical , genetics : DNA Primers, Exoribonucleases.
- chemical , metabolism : Exoribonucleases.
- chemical , pharmacology : Viral Vaccines.
- chemical , physiology : Exoribonucleases.
- drug therapy : Severe Acute Respiratory Syndrome.
- enzymology : SARS Virus.
- genetics : Plasmids, SARS Virus.
- immunology : Immunocompromised Host, Severe Acute Respiratory Syndrome.
- pathogenicity : SARS Virus.
- physiology : Virus Replication.
- virology : Severe Acute Respiratory Syndrome.
- Age Factors, Animals, Base Sequence, Drug Design, Female, Mice, Mice, Inbred BALB C, Molecular Sequence Data, Real-Time Polymerase Chain Reaction, Sequence Analysis, DNA, Statistics, Nonparametric.
Abstract
Live, attenuated RNA virus vaccines are efficacious but subject to reversion to virulence. Among RNA viruses, replication fidelity is recognized as a key determinant of virulence and escape from antiviral therapy; increased fidelity is attenuating for some viruses. Coronavirus (CoV) replication fidelity is approximately 20-fold greater than that of other RNA viruses and is mediated by a 3'→5' exonuclease (ExoN) activity that probably functions in RNA proofreading. In this study we demonstrate that engineered inactivation of severe acute respiratory syndrome (SARS)-CoV ExoN activity results in a stable mutator phenotype with profoundly decreased fidelity in vivo and attenuation of pathogenesis in young, aged and immunocompromised mice. The ExoN inactivation genotype and mutator phenotype are stable and do not revert to virulence, even after serial passage or long-term persistent infection in vivo. ExoN inactivation has potential for broad applications in the stable attenuation of CoVs and, perhaps, other RNA viruses.
DOI: 10.1038/nm.2972
PubMed: 23142821
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pubmed:23142821Le document en format XML
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type="abstract" xml:lang="en">Live, attenuated RNA virus vaccines are efficacious but subject to reversion to virulence. Among RNA viruses, replication fidelity is recognized as a key determinant of virulence and escape from antiviral therapy; increased fidelity is attenuating for some viruses. Coronavirus (CoV) replication fidelity is approximately 20-fold greater than that of other RNA viruses and is mediated by a 3'→5' exonuclease (ExoN) activity that probably functions in RNA proofreading. In this study we demonstrate that engineered inactivation of severe acute respiratory syndrome (SARS)-CoV ExoN activity results in a stable mutator phenotype with profoundly decreased fidelity in vivo and attenuation of pathogenesis in young, aged and immunocompromised mice. The ExoN inactivation genotype and mutator phenotype are stable and do not revert to virulence, even after serial passage or long-term persistent infection in vivo. ExoN inactivation has potential for broad applications in the stable attenuation of CoVs and, perhaps, other RNA viruses.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23142821</PMID><DateCompleted><Year>2013</Year><Month>02</Month><Day>11</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1546-170X</ISSN><JournalIssue CitedMedium="Internet"><Volume>18</Volume><Issue>12</Issue><PubDate><Year>2012</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Nature medicine</Title><ISOAbbreviation>Nat. Med.</ISOAbbreviation></Journal><ArticleTitle>A live, impaired-fidelity coronavirus vaccine protects in an aged, immunocompromised mouse model of lethal disease.</ArticleTitle><Pagination><MedlinePgn>1820-6</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/nm.2972</ELocationID><Abstract><AbstractText>Live, attenuated RNA virus vaccines are efficacious but subject to reversion to virulence. Among RNA viruses, replication fidelity is recognized as a key determinant of virulence and escape from antiviral therapy; increased fidelity is attenuating for some viruses. Coronavirus (CoV) replication fidelity is approximately 20-fold greater than that of other RNA viruses and is mediated by a 3'→5' exonuclease (ExoN) activity that probably functions in RNA proofreading. In this study we demonstrate that engineered inactivation of severe acute respiratory syndrome (SARS)-CoV ExoN activity results in a stable mutator phenotype with profoundly decreased fidelity in vivo and attenuation of pathogenesis in young, aged and immunocompromised mice. The ExoN inactivation genotype and mutator phenotype are stable and do not revert to virulence, even after serial passage or long-term persistent infection in vivo. ExoN inactivation has potential for broad applications in the stable attenuation of CoVs and, perhaps, other RNA viruses.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Graham</LastName><ForeName>Rachel L</ForeName><Initials>RL</Initials><AffiliationInfo><Affiliation>Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Becker</LastName><ForeName>Michelle M</ForeName><Initials>MM</Initials></Author><Author ValidYN="Y"><LastName>Eckerle</LastName><ForeName>Lance D</ForeName><Initials>LD</Initials></Author><Author ValidYN="Y"><LastName>Bolles</LastName><ForeName>Meagan</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Denison</LastName><ForeName>Mark R</ForeName><Initials>MR</Initials></Author><Author ValidYN="Y"><LastName>Baric</LastName><ForeName>Ralph 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