ArticlePoultry science2026
PTEN restricts infectious bursal disease virus replication through modulating the AKT-TBK1-mediated type I IFN pathway.
Article in Poultry science, 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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Abstract
PTEN, a canonical dual-specificity tumor suppressor, plays a pivotal role in regulating diverse physiological and pathological processes, including cell proliferation, apoptosis, and immune responses. Infectious bursal disease virus (IBDV) causes an acute, severe immunosuppressive disease in chickens, inflicting catastrophic economic losses on the poultry industry. Although PTEN has been shown to participate in host immunity, its specific role and underlying mechanism in avian defense against IBDV remain poorly understood. In this study, using chicken DF-1 cells and HD-11 cells as experimental models, we systematically investigated the regulatory effects of PTEN on IBDV replication. Bioinformatics analysis revealed that chicken PTEN shares the highest sequence homology with mallard duck PTEN, possessing highly conserved N-terminal phosphatase, C2, and C-terminal domains, with a widespread subcellular distribution across the cytoplasm, nucleus, and mitochondria. In vitro infection assays demonstrated that IBDV challenge significantly up-regulated both the mRNA and protein levels of PTEN in a time-dependent manner. Furthermore, confocal immunofluorescence microscopy revealed that IBDV infection induced a distinct nuclear translocation of PTEN. Further studies showed that PTEN overexpression markedly suppressed IBDV proliferation in a dose-dependent manner, whereas siRNA-mediated knockdown of endogenous PTEN significantly facilitated viral replication. Mechanistically, PTEN suppressed AKT activation to relieve its inhibitory effect on TBK1, thereby robustly enhancing the transcription of type I interferons and downstream interferon-stimulated genes. Taken together, our findings unveil a novel mechanism by which PTEN restricts IBDV replication via activation of the type I IFN pathway, providing fresh theoretical insights and a potential therapeutic target for the prevention and control of IBDV infection.
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