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DNA intercalator stimulates influenza transcription and virus replication

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 tr...

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Published in:Virology journal 2011-03, Vol.8 (1), p.120-120, Article 120
Main Authors: Li, Olive T W, Poon, Leo L M
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description 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)).
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subjects Animals
Cell Line
Clathrate compounds
Cyclin-dependent kinases
Dactinomycin - pharmacology
Experiments
Gene expression
Gene Expression Regulation, Viral - drug effects
Genetic aspects
Genetic transcription
Humans
Infections
Influenza
Influenza A virus - drug effects
Influenza A virus - enzymology
Influenza A virus - genetics
Influenza A virus - physiology
Influenza viruses
Influenza, Human - virology
Intercalating Agents - pharmacology
Kinases
Phosphorylation
Plasmids
Proteins
RNA Polymerase II - antagonists & inhibitors
RNA Polymerase II - genetics
RNA Polymerase II - metabolism
Short Report
Transcription, Genetic - drug effects
Viral infections
Viral Proteins - antagonists & inhibitors
Viral Proteins - genetics
Viral Proteins - metabolism
Virus Replication - drug effects
Viruses
title DNA intercalator stimulates influenza transcription and virus replication
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