{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["35(1)"],"submitter":["Chen B"],"pubmed_abstract":["Enterovirus A71 (EV-A71) is the major pathogen responsible for the severe hand, foot and mouth disease worldwide, for which few effective antiviral drugs are presently available. Interferon-α (IFN-α) has been used in antiviral therapy for decades; it has been reported that EV-A71 antagonizes the antiviral activity of IFN-α based on viral 2A<sup>pro</sup>-mediated reduction of the interferon-alpha receptor 1 (IFNAR1); however, the mechanism remains unknown. Here, we showed a significant increase in IFNAR1 protein induced by IFN-α in RD cells, whereas EV-A71 infection caused obvious down-regulation of the IFNAR1 protein and blockage of IFN-α signaling. Subsequently, we observed that EV-A71 2A<sup>pro</sup> inhibited IFNAR1 translation by cleavage of the eukaryotic initiation factor 4GI (eIF4"],"journal":["Virologica Sinica"],"pagination":["64-72"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7035401"],"repository":["biostudies-literature"],"pubmed_title":["Cellular Caspase-3 Contributes to EV-A71 2A<sup>pro</sup>-Mediated Down-Regulation of IFNAR1 at the Translation Level."],"pmcid":["PMC7035401"],"pubmed_authors":["Peng Y","Wang S","Zhang H","Pei X","Wang Y","Chen B"],"additional_accession":[]},"is_claimable":false,"name":"Cellular Caspase-3 Contributes to EV-A71 2A<sup>pro</sup>-Mediated Down-Regulation of IFNAR1 at the Translation Level.","description":"Enterovirus A71 (EV-A71) is the major pathogen responsible for the severe hand, foot and mouth disease worldwide, for which few effective antiviral drugs are presently available. Interferon-α (IFN-α) has been used in antiviral therapy for decades; it has been reported that EV-A71 antagonizes the antiviral activity of IFN-α based on viral 2A<sup>pro</sup>-mediated reduction of the interferon-alpha receptor 1 (IFNAR1); however, the mechanism remains unknown. Here, we showed a significant increase in IFNAR1 protein induced by IFN-α in RD cells, whereas EV-A71 infection caused obvious down-regulation of the IFNAR1 protein and blockage of IFN-α signaling. Subsequently, we observed that EV-A71 2A<sup>pro</sup> inhibited IFNAR1 translation by cleavage of the eukaryotic initiation factor 4GI (eIF4","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Feb","modification":"2025-04-21T18:01:07.892Z","creation":"2020-09-14T07:17:24Z"},"accession":"S-EPMC7035401","cross_references":{"pubmed":["31512106"],"doi":["10.1007/s12250-019-00151-y"]}}