<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>98(2)</volume><submitter>Huang H</submitter><pubmed_abstract>Porcine deltacoronavirus (PDCoV) has caused enormous economic losses to the global pig industry. However, the immune escape mechanism of PDCoV remains to be fully clarified. Transcriptomic analysis revealed a high abundance of interferon (IFN)-induced protein with tetratricopeptide repeats 3 (IFIT3) transcripts after PDCoV infection, which initially implied a correlation between IFIT3 and PDCoV. Further studies showed that PDCoV nsp5 could antagonize the host type I interferon signaling pathway by cleaving IFIT3. We demonstrated that PDCoV nsp5 cleaved porcine IFIT3 (pIFIT3) at Gln-406. Similar cleavage of endogenous IFIT3 has also been observed in PDCoV-infected cells. The pIFIT3-Q406A mutant was resistant to nsp5-mediated cleavage and exhibited a greater ability to inhibit PDCoV infectio</pubmed_abstract><journal>Journal of virology</journal><pagination>e0168223</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10878044</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Porcine deltacoronavirus nsp5 antagonizes type I interferon signaling by cleaving IFIT3.</pubmed_title><pmcid>PMC10878044</pmcid><pubmed_authors>Lan T</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Zhao C</pubmed_authors><pubmed_authors>Li C</pubmed_authors><pubmed_authors>Zhao B</pubmed_authors><pubmed_authors>Lu H</pubmed_authors><pubmed_authors>Lei X</pubmed_authors><pubmed_authors>Huang H</pubmed_authors><pubmed_authors>Zhang X</pubmed_authors><pubmed_authors>Qin Y</pubmed_authors><pubmed_authors>Jin N</pubmed_authors><pubmed_authors>Sun W</pubmed_authors></additional><is_claimable>false</is_claimable><name>Porcine deltacoronavirus nsp5 antagonizes type I interferon signaling by cleaving IFIT3.</name><description>Porcine deltacoronavirus (PDCoV) has caused enormous economic losses to the global pig industry. However, the immune escape mechanism of PDCoV remains to be fully clarified. Transcriptomic analysis revealed a high abundance of interferon (IFN)-induced protein with tetratricopeptide repeats 3 (IFIT3) transcripts after PDCoV infection, which initially implied a correlation between IFIT3 and PDCoV. Further studies showed that PDCoV nsp5 could antagonize the host type I interferon signaling pathway by cleaving IFIT3. We demonstrated that PDCoV nsp5 cleaved porcine IFIT3 (pIFIT3) at Gln-406. Similar cleavage of endogenous IFIT3 has also been observed in PDCoV-infected cells. The pIFIT3-Q406A mutant was resistant to nsp5-mediated cleavage and exhibited a greater ability to inhibit PDCoV infectio</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Feb</publication><modification>2026-06-18T06:52:27.04Z</modification><creation>2025-04-19T07:36:09.042Z</creation></dates><accession>S-EPMC10878044</accession><cross_references><pubmed>38289117</pubmed><doi>10.1128/jvi.01682-23</doi></cross_references></HashMap>