Inhibition of Japanese encephalitis virus infection by the host zinc-finger antiviral protein

PLoS Pathogens
Hsin-Ping ChiuYi-Ling Lin

Abstract

CCCH-type zinc-finger antiviral protein (ZAP) is a host factor that restricts the infection of many viruses mainly through RNA degradation, translation inhibition and innate immune responses. So far, only one flavivirus, yellow fever virus, has been reported to be ZAP-resistant. Here, we investigated the antiviral potential of human ZAP (isoform ZAP-L and ZAP-S) against three flaviviruses, Japanese encephalitis virus (JEV), dengue virus (DENV) and Zika virus (ZIKV). Infection of JEV but not DENV or ZIKV was blocked by ZAP overexpression, and depletion of endogenous ZAP enhanced JEV replication. ZAP hampered JEV translation and targeted viral RNA for 3'-5' RNA exosome-mediated degradation. The zinc-finger motifs of ZAP were essential for RNA targeting and anti-JEV activity. JEV 3'-UTR, especially in the region with dumbbell structures and high content of CG dinucleotide, was mapped to bind ZAP and confer sensitivity to ZAP. In summary, we identified JEV as the first ZAP-sensitive flavivirus. ZAP may act as an intrinsic antiviral factor through specific RNA binding to fight against JEV infection.

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Citations

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Datasets Mentioned

BETA
KU501215
AF014161
GSE115747

Methods Mentioned

BETA
Confocal microscopy
transfection
immunoprecipitation
pull down
pull-down
CLIP-seq
PCR
RIP
in vitro transcription
electrophoresis

Software Mentioned

CLC Genomics Workbench
ImageJ
AVONA

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