<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>21(4)</volume><submitter>Yu M</submitter><pubmed_abstract>Subgroup J avian leukosis virus (ALV-J), a retrovirus, elicits immunosuppression and persistent infections in chickens. Although it is widely acknowledged that ALV-J can evade the host's innate immune defenses, the mechanisms behind this immune evasion remain elusive. N6-methyladenosine (m6A), the most prevalent internal RNA modification, plays a role in innate immune evasion. Our research identified ALV-J as an inefficient stimulator of innate immunity in vitro and in vivo, with its genomic RNA featuring m6A modifications predominantly in the envelope protein (Env) region and 3' untranslated region (3'UTR). To elucidate the functional consequences of m6A modification, we subsequently generated m6A-deficient ALV-J through its culturing in the DF-1 overexpressing fat mass and obesity-associ</pubmed_abstract><journal>PLoS pathogens</journal><pagination>e1013064</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12043233</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>N6-methyladenosine modification of the subgroup J avian leukosis viral RNAs attenuates host innate immunity via MDA5 signaling.</pubmed_title><pmcid>PMC12043233</pmcid><pubmed_authors>Fan W</pubmed_authors><pubmed_authors>Yu M</pubmed_authors><pubmed_authors>Liu P</pubmed_authors><pubmed_authors>Zhang L</pubmed_authors><pubmed_authors>Guo R</pubmed_authors><pubmed_authors>Liu Y</pubmed_authors><pubmed_authors>Zhang T</pubmed_authors><pubmed_authors>Wang S</pubmed_authors><pubmed_authors>Qi X</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Gao Y</pubmed_authors><pubmed_authors>Cui H</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Meng L</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Duan Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>N6-methyladenosine modification of the subgroup J avian leukosis viral RNAs attenuates host innate immunity via MDA5 signaling.</name><description>Subgroup J avian leukosis virus (ALV-J), a retrovirus, elicits immunosuppression and persistent infections in chickens. Although it is widely acknowledged that ALV-J can evade the host's innate immune defenses, the mechanisms behind this immune evasion remain elusive. N6-methyladenosine (m6A), the most prevalent internal RNA modification, plays a role in innate immune evasion. Our research identified ALV-J as an inefficient stimulator of innate immunity in vitro and in vivo, with its genomic RNA featuring m6A modifications predominantly in the envelope protein (Env) region and 3' untranslated region (3'UTR). To elucidate the functional consequences of m6A modification, we subsequently generated m6A-deficient ALV-J through its culturing in the DF-1 overexpressing fat mass and obesity-associ</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Apr</publication><modification>2026-04-08T19:49:24.188Z</modification><creation>2025-07-06T03:05:50.08Z</creation></dates><accession>S-EPMC12043233</accession><cross_references><pubmed>40198675</pubmed><doi>10.1371/journal.ppat.1013064</doi></cross_references></HashMap>