AI Article Synopsis

  • Influenza A virus (IAV) infection activates NF-κB transcription factors through the canonical pathway, influencing the immune response and viral replication.
  • Researchers investigated the role of noncanonical NF-κB signaling after IAV infection by analyzing the activation of p52 and RelB.
  • They found that the viral NS1 protein significantly hinders RIG-I-mediated activation of noncanonical NF-κB and reduces the expression of the target gene CCL19.

Article Abstract

Influenza A virus (IAV) infection of epithelial cells activates NF-κB transcription factors via the canonical NF-κB signaling pathway, which modulates both the antiviral immune response and viral replication. Since almost nothing is known so far about a function of noncanonical NF-κB signaling after IAV infection, we tested infected cells for activation of p52 and RelB. We show that the viral NS1 protein strongly inhibits RIG-I-mediated noncanonical NF-κB activation and expression of the noncanonical target gene CCL19.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3446553PMC
http://dx.doi.org/10.1128/JVI.00323-12DOI Listing

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