AI Article Synopsis
- Influenza's NS1 protein is crucial for the virus's ability to survive and thrive in its host by binding to double-stranded RNA (dsRNA) and suppressing the immune response.
- This study reveals that NS1 can also attach to cellular double-stranded DNA (dsDNA), which prevents the necessary transcription machinery from accessing the DNA.
- By inhibiting the expression of antiviral genes, this highlights a new method through which the influenza virus dodges the host's antiviral defenses and enhances its own replication.
Article Abstract
Influenza NS1 protein is an important virulence factor that is capable of binding double-stranded (ds) RNA and inhibiting dsRNA-mediated host innate immune responses. Here we show that NS1 can also bind cellular dsDNA. This interaction prevents loading of transcriptional machinery to the DNA, thereby attenuating IAV-mediated expression of antiviral genes. Thus, we identified a previously undescribed strategy, by which RNA virus inhibits cellular transcription to escape antiviral response and secure its replication.
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| http://dx.doi.org/10.1016/j.bbagrm.2016.09.005 | DOI Listing |
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