Key result
Longer ZAP isoforms better inhibited alphaviruses and HBV, while all four isoforms equally inhibited Ebola virus transcription and replication and enhanced type I IFN expression.
Why the study?
ZAP is an IFN-induced host factor that inhibits a wide range of viruses, but fully characterizing its antiviral mechanism and individual isoform capacities remained an open question.
The antiviral activities of ZAP isoforms vary depending on the target virus, with longer isoforms showing greater efficacy against alphaviruses and HBV.
ZAP isoform data are hypothesis-generating; leaves open isoform-selective antiviral strategies pending in vivo validation.
ZAP is an IFN-induced host factor that can inhibit a wide range of viruses, and there is great interest in fully characterizing its antiviral mechanism. This is the first study that defines the antiviral capacities of individual ZAP isoforms in the absence of endogenous ZAP expression and, hence, cross talk with other isoforms. Our data demonstrate that ZAP is expressed as four different forms: ZAPS, ZAPM, ZAPL, and ZAPXL. The longer ZAP isoforms better inhibit alphaviruses and HBV, while all isoforms equally inhibit Ebola virus transcription and replication. In addition, there is no difference in the abilities of ZAP isoforms to enhance the induction of type I IFN expression. Our results show that the full spectrum of ZAP activities can change depending on the virus target and the relative levels of basal expression and induction by IFN or infection.
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Li et al. (2019) studied Viral infection. ZAP isoforms (ZAPS, ZAPM, ZAPL, ZAPXL) vs. Other isoforms was evaluated on Antiviral capacity and induction of type I IFN expression. Longer ZAP isoforms better inhibited alphaviruses and HBV, while all four isoforms equally inhibited Ebola virus transcription and replication and enhanced type I IFN expression.
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