Influenza Virus Infection Induces the Nuclear Relocalization of the Hsp90 Co-Chaperone p23 and Inhibits the Glucocorticoid Receptor Response p23 Association with Influenza Virus Polymerase
2011

Influenza Virus Infection Affects the Glucocorticoid Receptor Response

publication 10 minutes Evidence: moderate

Author Information

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

Primary Institution: Institut Pasteur, Paris, France

Hypothesis

Does influenza virus infection alter the function of the glucocorticoid receptor through the p23 cochaperone?

Conclusion

Influenza virus infection inhibits glucocorticoid receptor-mediated gene transactivation, potentially through a p23-independent pathway.

Supporting Evidence

  • p23 relocalizes to the nucleus in influenza virus-infected cells.
  • Viral infection impairs glucocorticoid receptor-mediated gene transactivation.
  • p23 is not essential for viral multiplication in cultured cells.
  • Influenza virus infection alters the glucocorticoid receptor's response to hormones.

Takeaway

When the flu virus infects cells, it can mess with how a hormone receptor works, which might make it harder for the body to respond to stress.

Methodology

The study used recombinant influenza viruses and various cell lines to analyze the interaction between the p23 cochaperone and the viral polymerase, as well as the effects on glucocorticoid receptor signaling.

Limitations

The study primarily focuses on cultured cells, which may not fully represent in vivo conditions.

Statistical Information

P-Value

p<0.02

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pone.0023368

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