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© Nadia Naffakh, Institut Pasteur
Immunofluorescence detection of influenza virus nucleoprotein in infected cells
Publication : PloS one

Influenza virus infection induces the nuclear relocalization of the Hsp90 co-chaperone p23 and inhibits the glucocorticoid receptor response.

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in PloS one - 10 Aug 2011

Ge X, Rameix-Welti MA, Gault E, Chase G, dos Santos Afonso E, Picard D, Schwemmle M, Naffakh N,

Link to Pubmed [PMID] – 21853119

Link to DOI – e2336810.1371/journal.pone.0023368

PLoS One 2011 ; 6(8): e23368

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.