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Updated: Jan 15, 2026

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
Avian leukosis virus subgroup J evades innate immunity by activating miR-155 to dually target TRAF3 and STAT1
Xinyue Zhang1, Defang Zhou1, Jing Zhou1
1College of Veterinary Medicine, Shandong Agricultural University, Tai'an City, Shandong Province, China.
Abstract:
Avian leukosis virus subgroup J (ALV-J) causes immunosuppression and myelocytomas in poultry. While ALV-J evades innate immunity to sustain infection, the mechanisms remain unclear. Here, we show that ALV-J upregulates microRNA-155 (miR-155) to suppress type I interferon (IFN-I) responses, facilitating viral replication. Mechanistically, the ALV-J p27 protein reduced DEAD-box helicase 3X (DDX3X) promoter activity, repressing its expression and promoting MIR155 host gene (MIR155HG) processing into mature miR-155. miR-155 directly targets the tumor necrosis factor receptor-associated factor 3 (TRAF3) and the signal transducer and activator of transcription 1 (STAT1), both of which are key regulators of IFN-I response. Silencing TRAF3 or STAT1 rescues ALV-J replication suppressed by miR-155 inhibition. These findings reveal a novel miRNA-mediated innate immune evasion strategy employed by ALV-J, enhancing our understanding of retroviral pathogenesis.
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