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- W1544415292 abstract "Influenza virus infections continue to represent a major public health threat. Influenza A virus virulence is multifactorial and requires an optimal constellation of viral genes in the context of a susceptible host. Interferons exert powerful antiviral effects against influenza viruses and are critical for host survival. Here we summarize recent progress in identifying viral and host factors which determine the outcome of infection, using highly pathogenic Asian H5N1 viruses or the pandemic 1918 ‘Spanish flu’ strain. Our infection models show that the full potential of type I and type III interferons against influenza viruses can only be appreciated in mice with a functional Mx1 gene being the main mediator of interferoninduced protection. Notably, common inbred mouse strains have defective Mx1 genes and, therefore, crippled innate defenses. Mx1 mouse models further revealed that IFN- , IFN- and IFN- contribute to resistance against influenza virus, and that animals lacking type I and type III IFN receptors are virtually defenseless. Influenza A viruses, in turn, evolved non-structural protein NS1 as an IFN antagonist and display diverse evasion mechanisms to escape the interferon system. Interestingly, a high virus multiplication speed may simply outrun the time-consuming establishment of the antiviral responses in immunocompetent Mx1-positive hosts." @default.
- W1544415292 created "2016-06-24" @default.
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- W1544415292 date "2008-01-01" @default.
- W1544415292 modified "2023-09-25" @default.
- W1544415292 title "Influenza A Virus Virulence and Innate Immunity: Recent Insights from New Mouse Models" @default.
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- W1544415292 doi "https://doi.org/10.1159/000151621" @default.
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