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Club cells surviving influenza A virus infection induce temporary nonspecific antiviral immunity.


ABSTRACT: A brief window of antigen-nonspecific protection has been observed after influenza A virus (IAV) infection. Although this temporary immunity has been assumed to be the result of residual nonspecific inflammation, this period of induced immunity has not been fully studied. Because IAV has long been characterized as a cytopathic virus (based on its ability to rapidly lyse most cell types in culture), it has been a forgone conclusion that directly infected cells could not be contributing to this effect. Using a Cre recombinase-expressing IAV, we have previously shown that club cells can survive direct viral infection. We show here not only that these cells can eliminate all traces of the virus and survive but also that they acquire a heightened antiviral response phenotype after surviving. Moreover, we experimentally demonstrate temporary nonspecific viral immunity after IAV infection and show that surviving cells are required for this phenotype. This work characterizes a virally induced modulation of the innate immune response that may represent a new mechanism to prevent viral diseases.

SUBMITTER: Hamilton JR 

PROVIDER: S-EPMC4833272 | biostudies-literature | 2016 Apr

REPOSITORIES: biostudies-literature

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Club cells surviving influenza A virus infection induce temporary nonspecific antiviral immunity.

Hamilton Jennifer R JR   Sachs David D   Lim Jean K JK   Langlois Ryan A RA   Palese Peter P   Heaton Nicholas S NS  

Proceedings of the National Academy of Sciences of the United States of America 20160321 14


A brief window of antigen-nonspecific protection has been observed after influenza A virus (IAV) infection. Although this temporary immunity has been assumed to be the result of residual nonspecific inflammation, this period of induced immunity has not been fully studied. Because IAV has long been characterized as a cytopathic virus (based on its ability to rapidly lyse most cell types in culture), it has been a forgone conclusion that directly infected cells could not be contributing to this ef  ...[more]

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