IFNAR1 and Herpesviridae infectious disease: Consistent with IFN contributing to an increase in ZBP1, we also note elevation of ZBP1 in primary fibroblasts following HSV1 infection; however, where IFN is essential for influenza-induced necroptosis, elimination of IFNAR signaling did not prevent ZBP1-induced necroptosis in the context of herpesvirus infection.