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. Author manuscript; available in PMC: 2015 Feb 6.
Published in final edited form as: Annu Rev Immunol. 2014 Feb 6;32:513–545. doi: 10.1146/annurev-immunol-032713-120231

Figure 4.

Figure 4

Targets for interferon (IFN)-stimulated proteins within viral life cycles. IFN-stimulated gene (ISG) products (stars) interfere with different stages of different viral life cycles. Cholesterol-25-hydroxylase (CH25H) affects viruses early, presumably at the host-membrane fusion event; at protein maturation of viral structural proteins by prenylation; and at protein maturation of viral replication enzymes. IFN-induced transmembrane (IFITM) protein members inhibit endocytic-fusion events of a broad spectrum of viruses. Tripartite motif protein 5 α (TRIM5 α) inhibits human immunodeficiency virus 1 (HIV-1) uncoating of the viral RNA. The myxoma resistance protein 1 (Mx1) inhibits a wide range of viruses by blocking endocytic traffic of incoming virus particles and uncoating of ribonucleocapsids. Some ISGs inhibit viruses by degrading viral RNA and/or blocking translation of viral mRNAs, such as 2′,5′-oligoadenylate synthetase (OAS) and latent ribonuclease L (RNase L), protein kinase R (PKR), Moloney leukemia virus 10 homolog (MOV10), and zinc-finger antiviral protein (ZAP). IFN-induced proteins with tetratricopeptide repeats (IFIT) inhibit protein translation and have been implicated in viral RNA degradation as well. TRIM22 inhibits viral transcription, replication, or trafficking of viral proteins to the plasma membrane. ISG15 can inhibit viral translation, replication, or egress. Viperin has been shown to inhibit viral replication or virus budding at the plasma membrane. Finally, tetherin traps otherwise mature virus particles on the plasma membrane and thus inhibits viral release, exerting its effect broadly on many enveloped viruses.