Skip to main content
. Author manuscript; available in PMC: 2021 Sep 29.
Published in final edited form as: Annu Rev Virol. 2020 Jun 30;7(1):421–446. doi: 10.1146/annurev-virology-011720-095930

Figure 3.

Figure 3

Reported inhibitory mechanisms of viral infections by viperin. Viperin localizes on the cytosolic face of the ER and to LDs, both of which often serve as platforms for viral RCs. Viperin catalyzes the conversion of CTP, possibly produced by CMPK2, to ddhCTP, which serves as a chain terminator during flavivirus replication. Viperin can also promote viral protein degradation, bind to proteins from several different viruses, and interfere with Golgi-dependent trafficking of soluble proteins and promote the release of immature capsids through sequestration of the host factor GBF1. Viperin can inhibit cholesterol synthesis through binding to FPPS, resulting in disruption of lipid rafts at the plasma membrane used by some viruses during their egress. Abbreviations: CMPK2, cytidylate monophosphate kinase 2; CTP, cytidine triphosphate; ddhCTP, 3′-deoxy-3′,4′-didehydro-cytidine triphosphate; DENV, dengue virus; ER, endoplasmic reticulum; EV-A71, enterovirus A71; FPPS, farnesyl diphosphate synthase; GBF1, Golgi-specific brefeldin A-resistance guanine nucleotide exchange factor 1; HCV, hepatitis C virus; HIV, human immunodeficiency virus; IAV, influenza A virus; JEV, Japanese encephalitis virus; LD, lipid droplet; RC, replication complex; TBEV, tick-borne encephalitis virus; WNV, West Nile virus; ZIKV, Zika virus.