Middle East respiratory syndrome and severe acute respiratory syndrome.
Identifieur interne : 001268 ( PubMed/Corpus ); précédent : 001267; suivant : 001269Middle East respiratory syndrome and severe acute respiratory syndrome.
Auteurs : Rahul Vijay ; Stanley PerlmanSource :
- Current opinion in virology [ 1879-6265 ] ; 2016.
English descriptors
- KwdEn :
- Animals, Coronavirus Infections (immunology), Coronavirus Infections (metabolism), Coronavirus Infections (transmission), Coronavirus Infections (virology), Disease Susceptibility, Epitopes (immunology), Host-Pathogen Interactions (immunology), Humans, Immunomodulation, Middle East Respiratory Syndrome Coronavirus (physiology), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (metabolism), Severe Acute Respiratory Syndrome (virology), T-Lymphocyte Subsets (immunology), T-Lymphocyte Subsets (metabolism).
- MESH :
- chemical , immunology : Epitopes.
- immunology : Coronavirus Infections, Host-Pathogen Interactions, Severe Acute Respiratory Syndrome, T-Lymphocyte Subsets.
- metabolism : Coronavirus Infections, Severe Acute Respiratory Syndrome, T-Lymphocyte Subsets.
- physiology : Middle East Respiratory Syndrome Coronavirus.
- transmission : Coronavirus Infections.
- virology : Coronavirus Infections, Severe Acute Respiratory Syndrome.
- Animals, Disease Susceptibility, Humans, Immunomodulation.
Abstract
The recent emergence of the Middle East respiratory syndrome (MERS)-CoV, a close relative of the Severe Acute respiratory syndrome (SARS)-CoV, both of which caused a lethal respiratory infection in humans, reinforces the need for further understanding of coronavirus pathogenesis and the host immune response. These viruses have evolved diverse strategies to evade and block host immune responses, facilitating infection and transmission. Pathogenesis following infection with these viruses is characterized by a marked delay in the induction of Type I interferon (IFN I) and, subsequently, by a poor adaptive immune response. Therapies that expedite IFN I induction as well as interventions that antagonize immunoevasive virus proteins are thus promising candidates for immune modulation.
DOI: 10.1016/j.coviro.2016.01.011
PubMed: 26855039
Links to Exploration step
pubmed:26855039Le document en format XML
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These viruses have evolved diverse strategies to evade and block host immune responses, facilitating infection and transmission. Pathogenesis following infection with these viruses is characterized by a marked delay in the induction of Type I interferon (IFN I) and, subsequently, by a poor adaptive immune response. Therapies that expedite IFN I induction as well as interventions that antagonize immunoevasive virus proteins are thus promising candidates for immune modulation. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26855039</PMID><DateCompleted><Year>2016</Year><Month>12</Month><Day>19</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1879-6265</ISSN><JournalIssue CitedMedium="Internet"><Volume>16</Volume><PubDate><Year>2016</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Current opinion in virology</Title><ISOAbbreviation>Curr Opin Virol</ISOAbbreviation></Journal><ArticleTitle>Middle East respiratory syndrome and severe acute respiratory syndrome.</ArticleTitle><Pagination><MedlinePgn>70-76</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S1879-6257(16)00014-6</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.coviro.2016.01.011</ELocationID><Abstract><AbstractText>The recent emergence of the Middle East respiratory syndrome (MERS)-CoV, a close relative of the Severe Acute respiratory syndrome (SARS)-CoV, both of which caused a lethal respiratory infection in humans, reinforces the need for further understanding of coronavirus pathogenesis and the host immune response. These viruses have evolved diverse strategies to evade and block host immune responses, facilitating infection and transmission. Pathogenesis following infection with these viruses is characterized by a marked delay in the induction of Type I interferon (IFN I) and, subsequently, by a poor adaptive immune response. Therapies that expedite IFN I induction as well as interventions that antagonize immunoevasive virus proteins are thus promising candidates for immune modulation. </AbstractText><CopyrightInformation>Copyright © 2016 Elsevier B.V. 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