ArticleAutophagy2026
African swine fever virus pE199L, as a mitophagy receptor, suppresses antiviral innate immunity to promote viral replication.
Article in Autophagy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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13 authors.
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Abstract
The African swine fever virus (ASFV) employs sophisticated strategies to promote viral replication in the host; however, the underlying mechanisms remain incompletely understood. Here, we demonstrated that the ASFV encoded pE199L protein acts as a potential mitophagy receptor that disrupted innate immunity through structural mimicry. The pE199L protein localized to mitochondria via its C terminal hydrophobic domain (155-199 aa) and induced mitochondrial fission by promoting DNM1L/Drp1 phosphorylation. Importantly, pE199L contained three LC3-interacting regions (LIRs: W35-I38, F157-L160, F193-L196) that directed autophagic degradation of key immune adaptors. Specifically, pE199L mediated mitophagic clearance of TBK1 (the CGAS-STING1 pathway) and MAVS (the RLR-MAVS pathway), thereby inhibiting type I interferon production and enhancing viral replication. This dual degradation mechanism was confirmed through rescue experiments using autophagy inhibitors and functional assays with LIR mutants. We identifted pE199L as the first canonical mitophagy receptor encoded by ASFV, unveiling a novel immune evasion strategy and a potential target for antiviral vaccine development.
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