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N6-methyladenosine modification of the subgroup J avian leukosis viral RNAs attenuates host innate immunity via MDA5 signaling

文献类型： 外文期刊

作者： Mengmeng Yu;Li Zhang;Ying Wang;Suyan Wang;Yongzhen Liu;Peng Liu;Yuntong Chen;Ru Guo;Lingzhai Meng;Tao Zhang;Wenrui Fan;Xiaole Qi;Yulu Duan;Yanping Zhang;Hongyu Cui;Yulong Gao

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关键词： 1

期刊名称： PLoS Pathogens

ISSN： 1553-7366

年卷期： 2025 年 21 卷 4 April 期

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收录情况： SCIE（2025版）

摘要： 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 (m6 A), 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 m6 A modifications predominantly in the envelope protein (Env) region and 3′ untranslated region (3′UTR). To elucidate the functional consequences of m6 A modification, we subsequently generated m6 A-deficient ALV-J through its culturing in the DF-1 overexpressing fat mass and obesityassociated protein (FTO) cells. The m6 A-deficient ALV-J virus, or its RNAs significantly enhanced IFN-β production compared to the wild-type (wt) ALV-J, suggesting a pivotal regulatory function of m6 A modifications in modulating innate immune response. Mechanistically, the m6 A modification of the ALV-J genomic RNA directly impacted its recognition by MDA5, weakening its binding and ubiquitination and attenuating IFN-β activation. Moreover, m6 A-deficient ALV-J, created by inducing mutations in m6 A sites within Env and 3′UTR, exhibited reduced replication capacity and elevated IFN-β expression in host cells. Importantly, this phenomenon was abolished in MDA5-knockout DF-1 cells, further demonstrating the core role of MDA5. These data demonstrate that m6 A modification of ALV-J genomic RNA dampens the host’s innate immune response through MDA5 signaling pathway.

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