SrasV1, PubMed, Corpus, bibRecord, 001A17

Mechanisms of severe acute respiratory syndrome pathogenesis and innate immunomodulation.

Identifieur interne : 001A17 ( PubMed/Corpus ); précédent : 001A16; suivant : 001A18

Mechanisms of severe acute respiratory syndrome pathogenesis and innate immunomodulation.

Auteurs : Matthew Frieman ; Ralph Baric

Source :

Microbiology and molecular biology reviews : MMBR [ 1098-5557 ] ; 2008.

RBID : pubmed:19052324

English descriptors

KwdEn :
- Animals, Coronavirus (genetics), Coronavirus (physiology), Coronavirus Infections (virology), Genome, Viral (genetics), Humans, Immunity, Innate, SARS Virus (genetics), SARS Virus (immunology), SARS Virus (pathogenicity), Severe Acute Respiratory Syndrome (genetics), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (virology), Virus Replication.
MESH :
- genetics : Coronavirus, Genome, Viral, SARS Virus, Severe Acute Respiratory Syndrome.
- immunology : SARS Virus, Severe Acute Respiratory Syndrome.
- pathogenicity : SARS Virus.
- physiology : Coronavirus.
- virology : Coronavirus Infections, Severe Acute Respiratory Syndrome.
- Animals, Humans, Immunity, Innate, Virus Replication.

Abstract

The modulation of the immune response is a common practice of many highly pathogenic viruses. The emergence of the highly pathogenic coronavirus severe acute respiratory virus (SARS-CoV) serves as a robust model system to elucidate the virus-host interactions that mediate severe end-stage lung disease in humans and animals. Coronaviruses encode the largest positive-sense RNA genome of approximately 30 kb, encode a variety of replicase and accessory open reading frames that are structurally unique, and encode novel enzymatic functions among RNA viruses. These viruses have broad or specific host ranges, suggesting the possibility of novel strategies for targeting and regulating host innate immune responses following virus infection. Using SARS-CoV as a model, we review the current literature on the ability of coronaviruses to interact with and modify the host intracellular environment during infection. These studies are revealing a rich set of novel viral proteins that engage, modify, and/or disrupt host cell signaling and nuclear import machinery for the benefit of virus replication.

DOI: 10.1128/MMBR.00015-08
PubMed: 19052324

Links to Exploration step

pubmed:19052324

Le document en format XML

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<front><div type="abstract" xml:lang="en">The modulation of the immune response is a common practice of many highly pathogenic viruses. The emergence of the highly pathogenic coronavirus severe acute respiratory virus (SARS-CoV) serves as a robust model system to elucidate the virus-host interactions that mediate severe end-stage lung disease in humans and animals. Coronaviruses encode the largest positive-sense RNA genome of approximately 30 kb, encode a variety of replicase and accessory open reading frames that are structurally unique, and encode novel enzymatic functions among RNA viruses. These viruses have broad or specific host ranges, suggesting the possibility of novel strategies for targeting and regulating host innate immune responses following virus infection. Using SARS-CoV as a model, we review the current literature on the ability of coronaviruses to interact with and modify the host intracellular environment during infection. These studies are revealing a rich set of novel viral proteins that engage, modify, and/or disrupt host cell signaling and nuclear import machinery for the benefit of virus replication.</div>
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Mechanisms of severe acute respiratory syndrome pathogenesis and innate immunomodulation.

Mechanisms of severe acute respiratory syndrome pathogenesis and innate immunomodulation.

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