However, the potent induction of ISG20 during infection in the absence of detectable IFN-β suggests that IFN-β-independent mechanisms likely play a major role in this process; (2) ISG20’s antiviral activity may manifest after viral entry and is most likely mediated at post-transcriptional level; (3) Overexpression of the viral large T antigen (LT) can bind to ISG20 and directly induce its expression. Here, ISG20 is linked to infection.