Abstract
Influenza A virus uses its host transcription machinery to facilitate viral RNA synthesis, an event that is associated with cellular RNA polymerase II (RNAPII). In this study, various RNAPII transcription inhibitors were used to investigate the effect of RNAPII phosphorylation status on viral RNA transcription. A low concentration of DNA intercalators, such as actinomycin D (ActD), was found to stimulate viral polymerase activity and virus replication. This effect was not observed in cells treated with RNAPII kinase inhibitors. In addition, the loss of RNAPII(a) in infected cells was due to the shift of nonphosphorylated RNAPII (RNAPII(a)) to hyperphosphorylated RNAPII (RNAPII(o)).
Publication types
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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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Dactinomycin / pharmacology
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Gene Expression Regulation, Viral / drug effects
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Humans
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Influenza A virus / drug effects*
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Influenza A virus / enzymology
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Influenza A virus / genetics*
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Influenza A virus / physiology
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Influenza, Human / virology
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Intercalating Agents / pharmacology*
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RNA Polymerase II / antagonists & inhibitors
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RNA Polymerase II / genetics
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RNA Polymerase II / metabolism
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Transcription, Genetic / drug effects*
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Viral Proteins / antagonists & inhibitors
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Viral Proteins / genetics
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Viral Proteins / metabolism
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Virus Replication / drug effects*
Substances
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Intercalating Agents
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Viral Proteins
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Dactinomycin
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RNA Polymerase II