Human Cell Tropism and Innate Immune System Interactions of Human Respiratory Coronavirus EMC Compared to Those of Severe Acute Respiratory Syndrome Coronavirus
Identifieur interne : 002625 ( Ncbi/Checkpoint ); précédent : 002624; suivant : 002626Human Cell Tropism and Innate Immune System Interactions of Human Respiratory Coronavirus EMC Compared to Those of Severe Acute Respiratory Syndrome Coronavirus
Auteurs : Florian Zielecki ; Michaela Weber ; Markus Eickmann ; Larissa Spiegelberg ; Ali Moh Zaki ; Mikhail Matrosovich ; Stephan Becker ; Friedemann WeberSource :
- Journal of Virology [ 0022-538X ] ; 2013.
Descripteurs français
- KwdFr :
- Animaux, Coronavirus (immunologie), Coronavirus (physiologie), Facteur-3 de régulation d'interféron (immunologie), Humains, Immunité innée, Infections à coronavirus (immunologie), Infections à coronavirus (virologie), Interféron de type I (immunologie), Lignée cellulaire, Primates, Réplication virale, Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (virologie), Tropisme viral, Virus du SRAS (immunologie), Virus du SRAS (physiologie).
- MESH :
- immunologie : Coronavirus, Facteur-3 de régulation d'interféron, Infections à coronavirus, Interféron de type I, Syndrome respiratoire aigu sévère, Virus du SRAS.
- physiologie : Coronavirus, Virus du SRAS.
- virologie : Infections à coronavirus, Syndrome respiratoire aigu sévère.
- Animaux, Humains, Immunité innée, Lignée cellulaire, Primates, Réplication virale, Tropisme viral.
English descriptors
- KwdEn :
- Animals, Cell Line, Coronavirus (immunology), Coronavirus (physiology), Coronavirus Infections (immunology), Coronavirus Infections (virology), Humans, Immunity, Innate, Interferon Regulatory Factor-3 (immunology), Interferon Type I (immunology), Primates, SARS Virus (immunology), SARS Virus (physiology), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (virology), Viral Tropism, Virus Replication.
- MESH :
- chemical , immunology : Interferon Regulatory Factor-3, Interferon Type I.
- immunology : Coronavirus, Coronavirus Infections, SARS Virus, Severe Acute Respiratory Syndrome.
- physiology : Coronavirus, SARS Virus.
- virology : Coronavirus Infections, Severe Acute Respiratory Syndrome.
- Animals, Cell Line, Humans, Immunity, Innate, Primates, Viral Tropism, Virus Replication.
Abstract
Infections with human coronavirus EMC (HCoV-EMC) are associated with severe pneumonia. We demonstrate that HCoV-EMC resembles severe acute respiratory syndrome coronavirus (SARS-CoV) in productively infecting primary and continuous cells of the human airways and in preventing the induction of interferon regulatory factor 3 (IRF-3)-mediated antiviral alpha/beta interferon (IFN-α/β) responses. However, HCoV-EMC was markedly more sensitive to the antiviral state established by ectopic IFN. Thus, HCoV-EMC can utilize a broad range of human cell substrates and suppress IFN induction, but it does not reach the IFN resistance of SARS-CoV.
Url:
DOI: 10.1128/JVI.03496-12
PubMed: 23449793
PubMed Central: 3624328
Affiliations:
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PMC:3624328Le document en format XML
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<front><div type="abstract" xml:lang="en"><p>Infections with human coronavirus EMC (HCoV-EMC) are associated with severe pneumonia. We demonstrate that HCoV-EMC resembles severe acute respiratory syndrome coronavirus (SARS-CoV) in productively infecting primary and continuous cells of the human airways and in preventing the induction of interferon regulatory factor 3 (IRF-3)-mediated antiviral alpha/beta interferon (IFN-α/β) responses. However, HCoV-EMC was markedly more sensitive to the antiviral state established by ectopic IFN. Thus, HCoV-EMC can utilize a broad range of human cell substrates and suppress IFN induction, but it does not reach the IFN resistance of SARS-CoV.</p>
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