Phospholipase PLA2G16 Accelerates the Host Interferon Signaling Pathway Response to FMDV
文献类型: 外文期刊
第一作者: Sun, Bingjie
作者: Sun, Bingjie;Qin, Xiaodong;Zhang, Taoqing;Dong, Sujie;Ye, Yinbo;Wang, Changying;Zhang, Yan;Hao, Rongzeng;Ru, Yi;Tian, Hong;Zheng, Haixue
作者机构:
关键词: FMDV; STAT1 phosphorylation; innate immunity
期刊名称:VIRUSES-BASEL ( 影响因子:3.5; 五年影响因子:3.7 )
ISSN:
年卷期: 2025 年 17 卷 7 期
页码:
收录情况: SCI
摘要: PLA2G16 is a member of the phospholipase A2 family that catalyzes the generation of lysophosphatidic acids (LPAs) and free fatty acids (FFAs) from phosphatidic acid. Previously, PLA2G16 was found to be a host factor for picornaviruses. Here, we discovered that the Foot-and-Mouth Disease Virus (FMDV) infection led to an elevation in PLA2G16 transcription. We established PLA2G16 overexpression and knockdown cell lines in PK-15 cells to investigate the potential role of PLA2G16 in FMDV infection. Our findings revealed that during FMDV infection, PLA2G16-overexpressing cells had increased levels of phosphorylated STAT1 and the interferon-stimulating factors ISG15 and ISG56. In PLA2G16-overexpressing cells, p-STAT1 was observed at higher levels and earlier than in wild-type cells. Subsequent research demonstrated that PLA2G16 specifically promoted an antiviral innate immune response against FMDV. The host could detect the early release of FMDV viral nucleic acid in PLA2G16-overexpressing cells and trigger the interferon signaling pathway. Additionally, we discovered that the supernatants of PLA2G16-overexpressing cells stimulated the production of higher levels of ISG56 and phosphorylated STAT1. This suggests that PLA2G16-overexpressing cells can activate the innate immune pathway of uninfected cells after FMDV infection.
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