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. Author manuscript; available in PMC: 2022 Dec 1.
Published in final edited form as: Curr Opin Virol. 2021 Oct 21;51:134–140. doi: 10.1016/j.coviro.2021.10.004

Fig. 1. Z-RNA is a ZBP1-activating PAMP.

Fig. 1

A. Structures of the left- and right-handed conformations of dsRNA and dsDNA. The ‘handedness’ of each duplex, and their cellular receptors, are shown below each structure. B. Orthomyxoviruses (IAV/IBV) and poxviruses (VACV) produce Z-RNAs, which are sensed by ZBP1 in a manner requiring the second of its two Zα domains. VACV E3 contains a Zα domain and prevents ZBP1 activation by competing with ZBP1 for Z-RNA. ZBP1 activates the kinase RIPK3 via RHIM:RHIM interactions between these proteins. RIPK3 then activates parallel pathways of apoptosis and necroptosis in infected cells. Herpesviruses (MCMV, HSV-1/2) also activate ZBP1, but the ZBP1-triggering ligand(s) produced by these viruses is currently unknown. It remains to be seen if members of other virus families activate ZBP1, and if cellular sources of Z-RNA, for example those originating from transcription of endogenous retroviral elements (EREs), contribute to ZBP1 activation during acute infections.