STING single amino acid polymorphisms modulate iridovirus immune evasion and pathogenicity spectrum

• 成果类型: Article
• 署名作者: Qin, Xiaowei; Liang, Mincong; Pan, Weiqiang; Zhan, Zhipeng; Li, Chuanrui; You, Yanlin; Weng, Shaoping; He, Jianguo; Guo, Changjun
• 署名单位: Sun Yat Sen University; Southern Marine Science & Engineering Guangdong Laboratory; Southern Marine Science & Engineering Guangdong Laboratory (Zhuhai); Sun Yat Sen University
• 刊物名称: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
• ISSN/ISSBN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.2523268123
• 发表日期: 2026-01-27
• 页码: e2523268123
• 关键词: stimulator of interferon genes; iridovirus; immune evasion; single amino acid polymorphism; pathogenicity spectrum; CYTOSOLIC DNA SENSOR; INFECTIOUS SPLEEN; I-INTERFERON; intracellular dna; VIRUS ISKNV; protein; ubiquitination; degradation; virulence; receptor

摘要

The evolutionary arms race between viruses and hosts shapes host antiviral defenses and viral immune evasion, yet the mechanisms driving divergence in viral cross-species pathogenicity remain unclear. Here, we investigated the role of single amino acid polymorphisms (SAPs) in stimulator of interferon genes (STING) in modulating immune evasion ubiquitination at residues C196 and K315, promoting its degradation to suppress interferon responses. Importantly, the K315/R315 polymorphism acts as a molecular switch: lethality) vs. R315 in resistant species (<= 25% lethality). These findings suggest that the molecular mechanisms underlying the viral pathogenicity spectrum may be modulated in terms of biological diversity.