Influenza Virus Infection Induces the Nuclear Relocalization of the Hsp90 Co-Chaperone p23 and Inhibits the Glucocorticoid Receptor ResponseReport as inadecuate




Influenza Virus Infection Induces the Nuclear Relocalization of the Hsp90 Co-Chaperone p23 and Inhibits the Glucocorticoid Receptor Response - Download this document for free, or read online. Document in PDF available to download.

The genomic RNAs of influenza A viruses are associated with the viral polymerase subunits PB1, PB2, PA and nucleoprotein NP, forming ribonucleoprotein complexes RNPs. Transcription-replication of the viral genome occurs in the nucleus of infected cells. A role for Hsp90 in nuclear import and assembly of newly synthetized RNA-polymerase subunits has been proposed. Here we report that the p23 cochaperone of Hsp90, which plays a major role in glucocorticoid receptor folding and function, associates with influenza virus polymerase. We show that p23 is not essential for viral multiplication in cultured cells but relocalizes to the nucleus in influenza virus-infected cells, which may alter some functions of p23 and Hsp90. Moreover, we show that influenza virus infection inhibits glucocorticoid receptor-mediated gene transactivation, and that this negative effect can occur through a p23-independent pathway. Viral-induced inhibition of the glucocorticoid receptor response might be of significant importance regarding the physiopathology of influenza infections in vivo.



Author: Xingyi Ge , Marie-Anne Rameix-Welti , Elyanne Gault , Geoffrey Chase, Emmanuel dos Santos Afonso, Didier Picard, Martin Schwemmle

Source: http://plos.srce.hr/



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