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.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cell Line
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Coronavirus / immunology
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Coronavirus / physiology*
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Coronavirus Infections / immunology*
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Coronavirus Infections / virology
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Humans
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Immunity, Innate*
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Interferon Regulatory Factor-3 / immunology
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Interferon Type I / immunology
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Primates
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Severe Acute Respiratory Syndrome / immunology*
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Severe Acute Respiratory Syndrome / virology
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Severe acute respiratory syndrome-related coronavirus / immunology
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Severe acute respiratory syndrome-related coronavirus / physiology*
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Viral Tropism*
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Virus Replication
Substances
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Interferon Regulatory Factor-3
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Interferon Type I