Journal
CELLULAR AND MOLECULAR LIFE SCIENCES
Volume 71, Issue 5, Pages 885-898Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00018-013-1479-x
Keywords
Influenza virus; Inflammation; Hemostasis; Innate immune sensors; PAR1; Plasminogen; Fibrinolysis; HLA-G
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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.
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