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Switch from protective to adverse inflammation during influenza: viral determinants and hemostasis are caught as culprits

tetano

Editor, Senior Moderator
Cell Mol Life Sci. 2013 Oct 4. [Epub ahead of print]
Switch from protective to adverse inflammation during influenza: viral determinants and hemostasis are caught as culprits.
Berri F, L? VB, Jandrot-Perrus M, Lina B, Riteau B.
Source

VirPath, EA4610 Virologie et Pathologie Humaine, Facult? de m?decine RTH Laennec, Universit? Claude Bernard Lyon 1, Universit? de Lyon, 69008, Lyon, France.
Abstract

Influenza viruses cause acute respiratory infections, which are highly contagious and occur as seasonal epidemic and sporadic pandemic outbreaks. Innate immune response is activated shortly after infection with influenza A viruses (IAV), affording effective protection of the host. However, this response should be tightly regulated, as insufficient inflammation may result in virus escape from immunosurveillance. In contrast, excessive inflammation may result in bystander lung tissue damage, loss of respiratory capacity, and deterioration of the clinical outcome of IAV infections. In this review, we give a comprehensive overview of the innate immune response to IAV infection and summarize the most important findings on how the host can inappropriately respond to influenza.

PMID:
24091817
[PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/pubmed/24091817
 
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