Sabotage of antiviral signaling and effectors by influenza viruses.
Vertebrate cells activate multiple signaling modules upon virus infection to eliminate the invading pathogen and to prevent the establishment of a persistent infection. A major immediate response pathway is controlled by the RNA helicases RIG-I and MDA5, which, after recognition of viral nucleic acids, signal induction of the interferon (IFN)-alpha/beta cytokine family that upregulates numerous antiviral effector proteins. Virulent viruses, in contrast, have learned during co-evolution with their hosts to manipulate or avoid this response in order to prevail in a repulsive environment. Focusing on the influenza viruses and their IFN-antagonistic NS1 proteins, we summarize recent progress in this rapidly evolving field at the intersection of virology and immunobiology involving studies of how viral pathogens induce and sabotage cellular defenses.
Wolff
Thorsten
T
Robert Koch-Institut, Projektgruppe P15, Nordufer 20, D-13353 Berlin, Germany. wolfft@rki.de
Zielecki
Florian
F
Abt
Marion
M
Voss
Daniel
D
Semmler
Ilia
I
Matthaei
Markus
M
D000818:Animals; D006801:Humans; D050838:Interferon Regulatory Factor-3 / Q000276:immunology / Q000378:metabolism*; D007370:Interferon Type I / Q000276:immunology / Q000378:metabolism*; D009975:Orthomyxoviridae / Q000276:immunology / Q000378:metabolism*; D020365:RNA Helicases / Q000276:immunology / Q000378:metabolism*; D015398:Signal Transduction / Q000276:immunology; D017361:Viral Nonstructural Proteins / Q000276:immunology / Q000378:metabolism*
C085820:INS1 protein, influenza virus; D050838:Interferon Regulatory Factor-3; D007370:Interferon Type I; D017361:Viral Nonstructural Proteins; D020365:RNA Helicases