Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Influenza viruses induce a host shut off mechanism leading to the general inhibition of host gene expression in infected cells. Here, we report that the large subunit of host RNA polymerase II (Pol II) is degraded in infected cells and propose that this degradation is mediated by the viral RNA polymerase that associates with Pol II. We detect increased ubiquitylation of Pol II in infected cells and upon the expression of the viral RNA polymerase suggesting that the proteasome pathway plays a role in Pol II degradation. Furthermore, we find that expression of the viral RNA polymerase results in the inhibition of Pol II transcription. We propose that Pol II inhibition and degradation in influenza virus infected cells could represent a viral strategy to evade host antiviral defense mechanisms. Our results also suggest a mechanism for the temporal regulation of viral mRNA synthesis.

Original publication

DOI

10.1016/j.virol.2009.10.003

Type

Journal article

Journal

Virology

Publication Date

05/01/2010

Volume

396

Pages

125 - 134

Keywords

Cell Line, Humans, Influenza A virus, Promoter Regions, Genetic, RNA Polymerase II, RNA, Viral, Transcription, Genetic, Virus Replication