DNA intercalator stimulates influenza transcription and virus replication

• Published in: Virology journal 2011-03, Vol.8 (1), p.120-120, Article 120
• Main Authors: Li, Olive T W, Poon, Leo L M
• Format: Article
• Language: English
• 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
• ISSN: 1743-422X; 1743-422X
• DOI: 10.1186/1743-422X-8-120

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)).