<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Broto L</submitter><funding>Ministerio de Ciencia, Innovación y Universidades</funding><funding>MEC | Agencia Estatal de Investigación</funding><funding>Comunidad Autónoma de Madrid</funding><funding>Ministerio de Economía y Competitividad</funding><funding>Caixa Foundation</funding><pagination>JVI.02017-20</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8092823</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>95(5)</volume><pubmed_abstract>Infectious bursal disease virus (IBDV), the best characterized member of the &lt;i>Birnaviridae&lt;/i> family, is a highly relevant avian pathogen causing both acute and persistent infections in different avian hosts. Here, we describe the establishment of clonal, long-term, productive persistent IBDV infections in DF-1 chicken embryonic fibroblasts. Although virus yields in persistently-infected cells are exceedingly lower than those detected in acutely infected cells, the replication fitness of viruses isolated from persistently-infected cells is higher than that of the parental virus. Persistently-infected DF-1 and IBDV-cured cell lines derived from them do not respond to type I interferon (IFN). High-throughput genome sequencing revealed that this defect is due to mutations affecting the IFN</pubmed_abstract><journal>Journal of virology</journal><pubmed_title>Type I Interferon acts as a major barrier to the establishment of infectious bursal disease virus (IBDV) persistent infections.</pubmed_title><pmcid>PMC8092823</pmcid><funding_grant_id>FPU 18/01873</funding_grant_id><funding_grant_id>PEJD-2017-PRE/BIO-5006</funding_grant_id><funding_grant_id>AGL2017-87464-C2-1-P</funding_grant_id><funding_grant_id>AGL2014-60095-P</funding_grant_id><funding_grant_id>BES-2015-073589</funding_grant_id><pubmed_authors>Candelas-Rivera O</pubmed_authors><pubmed_authors>Rodriguez JR</pubmed_authors><pubmed_authors>Diaz-Beneitez E</pubmed_authors><pubmed_authors>Rodriguez D</pubmed_authors><pubmed_authors>Eterradossi N</pubmed_authors><pubmed_authors>Broto L</pubmed_authors><pubmed_authors>Fuentes D</pubmed_authors><pubmed_authors>Cubas-Gaona LL</pubmed_authors><pubmed_authors>Soubies SM</pubmed_authors><pubmed_authors>Romero N</pubmed_authors><pubmed_authors>Courtillon C</pubmed_authors><pubmed_authors>Mendez F</pubmed_authors><pubmed_authors>Rodriguez JF</pubmed_authors></additional><is_claimable>false</is_claimable><name>Type I Interferon acts as a major barrier to the establishment of infectious bursal disease virus (IBDV) persistent infections.</name><description>Infectious bursal disease virus (IBDV), the best characterized member of the &lt;i>Birnaviridae&lt;/i> family, is a highly relevant avian pathogen causing both acute and persistent infections in different avian hosts. Here, we describe the establishment of clonal, long-term, productive persistent IBDV infections in DF-1 chicken embryonic fibroblasts. Although virus yields in persistently-infected cells are exceedingly lower than those detected in acutely infected cells, the replication fitness of viruses isolated from persistently-infected cells is higher than that of the parental virus. Persistently-infected DF-1 and IBDV-cured cell lines derived from them do not respond to type I interferon (IFN). High-throughput genome sequencing revealed that this defect is due to mutations affecting the IFN</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Mar</publication><modification>2025-04-26T00:50:47.276Z</modification><creation>2022-02-11T05:51:44.354Z</creation></dates><accession>S-EPMC8092823</accession><cross_references><pubmed>33328313</pubmed><doi>10.1128/jvi.02017-20</doi><doi>10.1128/JVI.02017-20</doi></cross_references></HashMap>