Interestingly, this increase in infectious viral particle release does not appear to result from changes in IFN or inflammatory cytokine production as evidenced by the minimal production of IFN-β by astrocytes following infection, the lack of effect of STAT1 inhibition on PFU increases, and the lack of a significant effect of ZBP1 deficiency on HSV-1-induced release of this antiviral mediator or the key inflammatory cytokines IL-6 and TNF. The gene discussed is TNF; the disease is infection.