English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Influenza A virus remains a major public health concern, both in its annual toll in death and debilitation and its potential to cause devastating pandemics. Like any other virus, influenza A viruses are strongly dependent on cellular factors for replication. One of the hallmark signaling factors activated by viral pathogens is the transcription factor NF-κB. Activation of NF-κB leads to the up-regulation of a variety of antiviral genes. Thus, the factor is commonly regarded as a major regulator of the innate immune defense to infection. However, several recent studies indicate that influenza viruses have acquired the capability to reprogram this antiviral activity and to exploit the factor for efficient replication. These data provide novel insights into the pathophysiological function of NF-κB in the special environment of a virus-infected cell. Furthermore, the unexpected viral dependency on a cellular signaling factor may pave the path for novel antiviral approaches targeting essential cellular components rather than viral factors.

Influenza viruses and the NF-κB signaling pathway – towards a novel concept of antiviral therapy