Emerging Microbes and Infections · Available online 25 May 2026 · In press · DOI 10.1080/22221751.2026.2671465
Xuefei Sun, Min Zheng, Nan Li, Xiaoying Jia, Teng Chen, Shoufeng Zhang, Huixian Yue, Qixuan Li, Boli Ma, Fengjie Wang, Junnan Ke, Yiqian Jiang, Zhuo Hao, Rongliang Hu, Yanyan Zhang, Faming Miao
African swine fever (ASF) is a highly contagious and lethal disease caused by African swine fever virus (ASFV), with a mortality rate approaching up to 100%. At present, the functions of multiple genes of ASFV remain to be elucidated. In this study, we demonstrate that pD345L is a late-expressed viral protein and localizes to the viral factory. The recombinant strain JX23-02ΔD345L was obtained from the genotype I/II strain JX23-02. In vitro assays demonstrated that the deletion of D345L remarkably impairs viral replication. Further analyses revealed that JX23-02ΔD345L significantly up-regulated pro-inflammatory cytokines (IL-1β, TNF-α) and IFN pathway components in PAMs, induced pyroptosis, apoptosis, and interferon responses. In vivo animal experiments demonstrated that the JX23-02ΔD345L strain was completely attenuated in pigs, failing to induce any typical clinical signs of ASF even with a high-dose inoculation. Moreover, a single immunization with JX23-02ΔD345L can elicit specific humoral and cellular immune responses against ASFV, conferring 80% protection against intramuscular challenge with the homologous strain JX23-02 and 60% protection against the heterologous strain SY18. These results reveal D345L as a crucial virulence-related gene for ASFV pathogenesis, which is highly correlated with viral replication and the host antiviral response. Furthermore, JX23-02ΔD345L represented a candidate for the development of effective and safe ASFV vaccines. This finding provides a foundation for the research on ASFV and offers an important target and evidence for vaccine development.
Abstract from DOAJ. Public domain (CC0 1.0).
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Sun, X., Zheng, M., Li, N., et al. (2026). Deletion of the D345L gene attenuates ASFV and induces protection against homologous and heterologous challenge by enhancing host innate immunity. Emerging Microbes and Infections. https://doi.org/10.1080/22221751.2026.2671465