Abstract
Severe acute respiratory syndrome coronavirus (SARS-CoV) encodes several accessory proteins of unknown function. One of these proteins, protein 6 (p6), which is encoded by ORF6, enhances virus replication when introduced into a heterologous murine coronavirus (mouse hepatitis virus [MHV]) but is not essential for optimal SARS-CoV replication after infection at a relatively high multiplicity of infection (MOI). Here, we reconcile these apparently conflicting results by showing that p6 enhances SARS-CoV replication to nearly the same extent as when expressed in the context of MHV if cells are infected at a low MOI and accelerates disease in mice transgenic for the human SARS-CoV receptor.
Publication types
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Research Support, N.I.H., Extramural
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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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Interferon-gamma / pharmacology
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Mice
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Mice, Transgenic
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Open Reading Frames
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Receptors, Virus / metabolism
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STAT1 Transcription Factor / metabolism
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Severe Acute Respiratory Syndrome / virology
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Severe acute respiratory syndrome-related coronavirus / metabolism*
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Severe acute respiratory syndrome-related coronavirus / pathogenicity
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Severe acute respiratory syndrome-related coronavirus / physiology
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Viral Proteins / metabolism*
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Virus Replication*
Substances
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Receptors, Virus
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STAT1 Transcription Factor
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Stat1 protein, mouse
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Viral Proteins
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protein 6, SARS virus
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Interferon-gamma