We also found that the miR-183 cluster activates the IFN pathway and inhibits vesicular stomatitis virus (VSV) infection through direct targeting of several negative regulators of IRF3 and STAT1 activities, including protein phosphatase 2A (PPP2CA) and tripartite motif containing 27 (TRIM27).
In contrast, tumor-derived Pten(-/-) cells expressed higher levels of the antiviral transcription factor STAT1, activated STAT1 in response to VSV, and were resistant to VSV infection.