SrasV1, PubMed, Corpus, bibRecord, 000C82

SARS-like WIV1-CoV poised for human emergence.

Identifieur interne : 000C82 ( PubMed/Corpus ); précédent : 000C81; suivant : 000C83

SARS-like WIV1-CoV poised for human emergence.

Auteurs : Vineet D. Menachery ; Boyd L. Yount ; Amy C. Sims ; Kari Debbink ; Sudhakar S. Agnihothram ; Lisa E. Gralinski ; Rachel L. Graham ; Trevor Scobey ; Jessica A. Plante ; Scott R. Royal ; Jesica Swanstrom ; Timothy P. Sheahan ; Raymond J. Pickles ; Davide Corti ; Scott H. Randell ; Antonio Lanzavecchia ; Wayne A. Marasco ; Ralph S. Baric

Source :

Proceedings of the National Academy of Sciences of the United States of America [ 1091-6490 ] ; 2016.

RBID : pubmed:26976607

English descriptors

KwdEn :
- Animals, Antibodies, Monoclonal (immunology), Antibodies, Neutralizing (immunology), Antibodies, Viral (immunology), Cells, Cultured, Chiroptera (virology), Chlorocebus aethiops, Communicable Diseases, Emerging (virology), Coronaviridae (genetics), Coronaviridae (immunology), Coronaviridae (isolation & purification), Coronaviridae (pathogenicity), Coronaviridae (physiology), Coronaviridae Infections (prevention & control), Coronaviridae Infections (transmission), Coronaviridae Infections (veterinary), Coronaviridae Infections (virology), Cross Reactions, Encephalitis, Viral (virology), Epithelial Cells (virology), Host Specificity, Humans, Lung (cytology), Mice, Mice, Inbred BALB C, Mice, Transgenic, Models, Molecular, Peptidyl-Dipeptidase A (genetics), Peptidyl-Dipeptidase A (physiology), Point Mutation, Protein Conformation, Receptors, Virus (genetics), Receptors, Virus (physiology), Recombinant Fusion Proteins (metabolism), SARS Virus (immunology), Species Specificity, Spike Glycoprotein, Coronavirus (genetics), Spike Glycoprotein, Coronavirus (physiology), Vero Cells, Virus Replication, Zoonoses.
MESH :
- chemical , genetics : Peptidyl-Dipeptidase A, Receptors, Virus, Spike Glycoprotein, Coronavirus.
- chemical , immunology : Antibodies, Monoclonal, Antibodies, Neutralizing, Antibodies, Viral.
- cytology : Lung.
- genetics : Coronaviridae.
- immunology : Coronaviridae, SARS Virus.
- isolation & purification : Coronaviridae.
- chemical , metabolism : Recombinant Fusion Proteins.
- pathogenicity : Coronaviridae.
- physiology : Coronaviridae, Peptidyl-Dipeptidase A, Receptors, Virus, Spike Glycoprotein, Coronavirus.
- prevention & control : Coronaviridae Infections.
- transmission : Coronaviridae Infections.
- veterinary : Coronaviridae Infections.
- virology : Chiroptera, Communicable Diseases, Emerging, Coronaviridae Infections, Encephalitis, Viral, Epithelial Cells.
- Animals, Cells, Cultured, Chlorocebus aethiops, Cross Reactions, Host Specificity, Humans, Mice, Mice, Inbred BALB C, Mice, Transgenic, Models, Molecular, Point Mutation, Protein Conformation, Species Specificity, Vero Cells, Virus Replication, Zoonoses.

Abstract

Outbreaks from zoonotic sources represent a threat to both human disease as well as the global economy. Despite a wealth of metagenomics studies, methods to leverage these datasets to identify future threats are underdeveloped. In this study, we describe an approach that combines existing metagenomics data with reverse genetics to engineer reagents to evaluate emergence and pathogenic potential of circulating zoonotic viruses. Focusing on the severe acute respiratory syndrome (SARS)-like viruses, the results indicate that the WIV1-coronavirus (CoV) cluster has the ability to directly infect and may undergo limited transmission in human populations. However, in vivo attenuation suggests additional adaptation is required for epidemic disease. Importantly, available SARS monoclonal antibodies offered success in limiting viral infection absent from available vaccine approaches. Together, the data highlight the utility of a platform to identify and prioritize prepandemic strains harbored in animal reservoirs and document the threat posed by WIV1-CoV for emergence in human populations.

DOI: 10.1073/pnas.1517719113
PubMed: 26976607

Links to Exploration step

pubmed:26976607

Le document en format XML

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<author><name sortKey="Menachery, Vineet D" sort="Menachery, Vineet D" uniqKey="Menachery V" first="Vineet D" last="Menachery">Vineet D. Menachery</name>
<affiliation><nlm:affiliation>Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599;</nlm:affiliation>
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<author><name sortKey="Yount, Boyd L" sort="Yount, Boyd L" uniqKey="Yount B" first="Boyd L" last="Yount">Boyd L. Yount</name>
<affiliation><nlm:affiliation>Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599;</nlm:affiliation>
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<author><name sortKey="Sims, Amy C" sort="Sims, Amy C" uniqKey="Sims A" first="Amy C" last="Sims">Amy C. Sims</name>
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</affiliation>
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</affiliation>
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</affiliation>
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</affiliation>
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</affiliation>
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</affiliation>
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</affiliation>
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</affiliation>
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</affiliation>
</author>
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</affiliation>
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<term>Cells, Cultured</term>
<term>Chiroptera (virology)</term>
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<front><div type="abstract" xml:lang="en">Outbreaks from zoonotic sources represent a threat to both human disease as well as the global economy. Despite a wealth of metagenomics studies, methods to leverage these datasets to identify future threats are underdeveloped. In this study, we describe an approach that combines existing metagenomics data with reverse genetics to engineer reagents to evaluate emergence and pathogenic potential of circulating zoonotic viruses. Focusing on the severe acute respiratory syndrome (SARS)-like viruses, the results indicate that the WIV1-coronavirus (CoV) cluster has the ability to directly infect and may undergo limited transmission in human populations. However, in vivo attenuation suggests additional adaptation is required for epidemic disease. Importantly, available SARS monoclonal antibodies offered success in limiting viral infection absent from available vaccine approaches. Together, the data highlight the utility of a platform to identify and prioritize prepandemic strains harbored in animal reservoirs and document the threat posed by WIV1-CoV for emergence in human populations. </div>
</front>
</TEI>
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<DateCompleted><Year>2016</Year>
<Month>08</Month>
<Day>11</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>12</Month>
<Day>10</Day>
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<JournalIssue CitedMedium="Internet"><Volume>113</Volume>
<Issue>11</Issue>
<PubDate><Year>2016</Year>
<Month>Mar</Month>
<Day>15</Day>
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<Title>Proceedings of the National Academy of Sciences of the United States of America</Title>
<ISOAbbreviation>Proc. Natl. Acad. Sci. U.S.A.</ISOAbbreviation>
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<ArticleTitle>SARS-like WIV1-CoV poised for human emergence.</ArticleTitle>
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<Abstract><AbstractText>Outbreaks from zoonotic sources represent a threat to both human disease as well as the global economy. Despite a wealth of metagenomics studies, methods to leverage these datasets to identify future threats are underdeveloped. In this study, we describe an approach that combines existing metagenomics data with reverse genetics to engineer reagents to evaluate emergence and pathogenic potential of circulating zoonotic viruses. Focusing on the severe acute respiratory syndrome (SARS)-like viruses, the results indicate that the WIV1-coronavirus (CoV) cluster has the ability to directly infect and may undergo limited transmission in human populations. However, in vivo attenuation suggests additional adaptation is required for epidemic disease. Importantly, available SARS monoclonal antibodies offered success in limiting viral infection absent from available vaccine approaches. Together, the data highlight the utility of a platform to identify and prioritize prepandemic strains harbored in animal reservoirs and document the threat posed by WIV1-CoV for emergence in human populations. </AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Menachery</LastName>
<ForeName>Vineet D</ForeName>
<Initials>VD</Initials>
<AffiliationInfo><Affiliation>Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yount</LastName>
<ForeName>Boyd L</ForeName>
<Initials>BL</Initials>
<Suffix>Jr</Suffix>
<AffiliationInfo><Affiliation>Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sims</LastName>
<ForeName>Amy C</ForeName>
<Initials>AC</Initials>
<AffiliationInfo><Affiliation>Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Debbink</LastName>
<ForeName>Kari</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599; Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599;</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Agnihothram</LastName>
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SARS-like WIV1-CoV poised for human emergence.

SARS-like WIV1-CoV poised for human emergence.

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