SrasV1, PubMed, Corpus, bibRecord, 000F93

Systems approaches to Coronavirus pathogenesis.

Identifieur interne : 000F93 ( PubMed/Corpus ); précédent : 000F92; suivant : 000F94

Systems approaches to Coronavirus pathogenesis.

Auteurs : Alexandra Sch Fer ; Ralph S. Baric ; Martin T. Ferris

Source :

Current opinion in virology [ 1879-6265 ] ; 2014.

RBID : pubmed:24842079

English descriptors

KwdEn :
- Animals, Coronavirus (physiology), Coronavirus Infections (etiology), Coronavirus Infections (virology), Genetic Techniques, Genetics, Host-Pathogen Interactions, Humans, Systems Biology (methods).
MESH :
- etiology : Coronavirus Infections.
- methods : Systems Biology.
- physiology : Coronavirus.
- virology : Coronavirus Infections.
- Animals, Genetic Techniques, Genetics, Host-Pathogen Interactions, Humans.

Abstract

Coronaviruses comprise a large group of emergent human and animal pathogens, including the highly pathogenic SARS-CoV and MERS-CoV strains that cause significant morbidity and mortality in infected individuals, especially the elderly. As emergent viruses may cause episodic outbreaks of disease over time, human samples are limited. Systems biology and genetic technologies maximize opportunities for identifying critical host and viral genetic factors that regulate susceptibility and virus-induced disease severity. These approaches provide discovery platforms that highlight and allow targeted confirmation of critical targets for prophylactics and therapeutics, especially critical in an outbreak setting. Although poorly understood, it has long been recognized that host regulation of virus-associated disease severity is multigenic. The advent of systems genetic and biology resources provides new opportunities for deconvoluting the complex genetic interactions and expression networks that regulate pathogenic or protective host response patterns following virus infection. Using SARS-CoV as a model, dynamic transcriptional network changes and disease-associated phenotypes have been identified in different genetic backgrounds, leading to the promise of population-wide discovery of the underpinnings of Coronavirus pathogenesis.

DOI: 10.1016/j.coviro.2014.04.007
PubMed: 24842079

Links to Exploration step

pubmed:24842079

Le document en format XML

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<front><div type="abstract" xml:lang="en">Coronaviruses comprise a large group of emergent human and animal pathogens, including the highly pathogenic SARS-CoV and MERS-CoV strains that cause significant morbidity and mortality in infected individuals, especially the elderly. As emergent viruses may cause episodic outbreaks of disease over time, human samples are limited. Systems biology and genetic technologies maximize opportunities for identifying critical host and viral genetic factors that regulate susceptibility and virus-induced disease severity. These approaches provide discovery platforms that highlight and allow targeted confirmation of critical targets for prophylactics and therapeutics, especially critical in an outbreak setting. Although poorly understood, it has long been recognized that host regulation of virus-associated disease severity is multigenic. The advent of systems genetic and biology resources provides new opportunities for deconvoluting the complex genetic interactions and expression networks that regulate pathogenic or protective host response patterns following virus infection. Using SARS-CoV as a model, dynamic transcriptional network changes and disease-associated phenotypes have been identified in different genetic backgrounds, leading to the promise of population-wide discovery of the underpinnings of Coronavirus pathogenesis. </div>
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<ReferenceList><Reference><Citation>Crit Rev Immunol. 2013;33(5):435-76</Citation>
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<ReferenceList><Reference><Citation>J Med Virol. 2013 May;85(5):808-14</Citation>
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{{Explor lien
   |wiki=    Sante
   |area=    SrasV1
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   |type=    RBID
   |clé=     pubmed:24842079
   |texte=   Systems approaches to Coronavirus pathogenesis.
}}

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Systems approaches to Coronavirus pathogenesis.

Systems approaches to Coronavirus pathogenesis.

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