[Influenza viruses and intracellular signalling pathways].
It has been described in the last years that after influenza virus-infection a variety of intracellular signalling pathways have been induced. There are examples and suggestions how the viral replication cycle leads to the activation of intracellular signalling pathways. A variety of signalling pathways are activated after virus-infection as an alert-response against the invading pathogen that can be considered as an antiviral response of the host cell. Nevertheless, it was also shown, that viruses are able to suppress these cellular responses to assure their own replication. Moreover, viruses are also able to activate and misuse cellular signalling pathways for their own survival. The NF-kappaB signalling pathway is an excellent example of these sceneries. Activation of the NF-kappaB signalling pathway mediated by the virus can partially be blocked by the NS1 protein to suppress a strong antiviral IFN alpha/beta response. At the same time the virus takes advantage of the remaining NF-kappaB activity for virus related apoptosis and for its own replication. This is a highly effective and economic way for the virus to control its replication without the need for specific viral inducers of cellular responses. This demonstrates, that there are no "all or nothing" reactions in the field of interactions of Influenza viruses with intracellular signalling pathways. In one situation cellular antiviral responses can be misused by the virus of its own replication and at another point the same signalling pathway may even be turned into a pro-viral activity. When the impact of a given signalling pathway on viral growth is evaluated these bivalent functions of these pathways should be taken in consideration. Nevertheless, a signalling pathway that supports viral growth is an excellent target for antiviral therapy (Ludwig et al. 2003).
Planz
Oliver
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Friedrich-Loeffler-lnstitut, Bundesforschungsinstitut für Tiergesundheit, Institut für Immunologie,Tübingen, Germany. oliver.planz@fli.bund.de
D000818:Animals; D017209:Apoptosis / Q000502:physiology; D006801:Humans; D007370:Interferon Type I / Q000502:physiology; D020928:Mitogen-Activated Protein Kinases / Q000502:physiology; D016328:NF-kappa B / Q000502:physiology; D009975:Orthomyxoviridae / Q000254:growth & development / Q000472:pathogenicity / Q000502:physiology*; D011493:Protein Kinase C / Q000502:physiology; D015398:Signal Transduction / Q000276:immunology* / Q000502:physiology*; D017361:Viral Nonstructural Proteins / Q000502:physiology; D014779:Virus Replication / Q000502:physiology*
C085820:INS1 protein, influenza virus; D007370:Interferon Type I; D016328:NF-kappa B; D017361:Viral Nonstructural Proteins; D011493:Protein Kinase C; D020928:Mitogen-Activated Protein Kinases