Please use this identifier to cite or link to this item: https://doi.org/10.1038/ncomms13150
Title: Human genome-wide RNAi screen reveals host factors required for enterovirus 71 replication
Authors: Wu, Kan Xing
PATCHARA PHUEKTES 
Kumar, Pankaj
Goh, Germaine Yen Lin
Moreau, Dimitri
CHOW TAK KWONG,VINCENT 
FREDERIC BARD 
CHU JANG HANN 
Keywords: Science & Technology
Multidisciplinary Sciences
Science & Technology - Other Topics
RIBOSOMAL ENTRY SITE
PEPTIDE-N-GLYCANASE
ERM PROTEINS
AURORA-B
INFECTION
BINDS
INHIBITOR
AUTOPHAGY
RECEPTOR
RADIXIN
Issue Date: 17-Oct-2016
Publisher: NATURE PUBLISHING GROUP
Citation: Wu, Kan Xing, PATCHARA PHUEKTES, Kumar, Pankaj, Goh, Germaine Yen Lin, Moreau, Dimitri, CHOW TAK KWONG,VINCENT, FREDERIC BARD, CHU JANG HANN (2016-10-17). Human genome-wide RNAi screen reveals host factors required for enterovirus 71 replication. NATURE COMMUNICATIONS 7 (1). ScholarBank@NUS Repository. https://doi.org/10.1038/ncomms13150
Abstract: © 2016 The Author(s). Enterovirus 71 (EV71) is a neurotropic enterovirus without antivirals or vaccine, and its host-pathogen interactions remain poorly understood. Here we use a human genome-wide RNAi screen to identify 256 host factors involved in EV71 replication in human rhabdomyosarcoma cells. Enrichment analyses reveal overrepresentation in processes like mitotic cell cycle and transcriptional regulation. We have carried out orthogonal experiments to characterize the roles of selected factors involved in cell cycle regulation and endoplasmatic reticulum-associated degradation. We demonstrate nuclear egress of CDK6 in EV71 infected cells, and identify CDK6 and AURKB as resistance factors. NGLY1, which co-localizes with EV71 replication complexes at the endoplasmatic reticulum, supports EV71 replication. We confirm importance of these factors for EV71 replication in a human neuronal cell line and for coxsackievirus A16 infection. A small molecule inhibitor of NGLY1 reduces EV71 replication. This study provides a comprehensive map of EV71 host factors and reveals potential antiviral targets.
Source Title: NATURE COMMUNICATIONS
URI: https://scholarbank.nus.edu.sg/handle/10635/170677
ISSN: 2041-1723
DOI: 10.1038/ncomms13150
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