Authors
Ying Wang, Shijin Lan, Zhenghui Fang, Shixing Yang, Xiaochun Wang, Quan Shen, Yuwei Liu, Ping Wu, Chenglin Zhou, Wen Zhang, Likai Ji
Published in
Transboundary and emerging diseases. Volume 2026. Issue 1. Pages e3676642.
Abstract
Porcine deltacoronavirus (PDCoV) is an emerging enteric coronavirus that causes substantial morbidity in swine and may pose a zoonotic risk because of its cross-species transmission potential. Type I interferon (IFN-I) signaling is central to antiviral defense, initiated through the mitochondrial antiviral signaling (MAVS)-TBK1-IFN regulatory factor 3 (IRF3) axis and executed by the downstream JAK-STAT1-STAT2-IRF9 (ISGF3) pathway; however, how PDCoV circumvents both the induction and effector arms of this cascade remains incompletely understood. Here, we identify PDCoV nonstructural protein 13 (Nsp13) as a potent antagonist of IFN-I responses. Ectopic expression of Nsp13 markedly reduces IFN-β production and the expression of IFN-stimulated genes (ISGs, such as ISG56 and CXCL10). Mechanistically, Nsp13 directly binds the C-terminal domain (CTD) of TBK1 and competitively disrupts TBK1 interactions with IRF3 and MAVS. In addition, Nsp13 preferentially binds IRF9 and impairs its nuclear translocation, thereby inhibiting IFN-α-induced signaling. Notably, PDCoV Nsp13 exhibits a host-target binding profile similar to that of SARS-CoV-2 Nsp13, yet it does not alter TBK1 ubiquitination or protein stability. Collectively, these findings reveal a dual-layer immune evasion strategy whereby PDCoV Nsp13 suppresses both IFN induction and downstream signaling, and highlighting Nsp13 as a potential target for antiviral intervention.
PMID:
42478070
Bibliographic data and abstract were imported from PubMed on 21 Jul 2026.
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