Sun Bingjie, Qin Xiaodong, Zhang Taoqing, Dong Sujie, Ye Yinbo, Wang Changying, Zhang Yan, Hao Rongzeng, Ru Yi, Tian Hong, Zheng Haixue
State Key Laboratory for Animal Disease Control and Prevention, National Foot and Mouth Disease Reference Laboratory, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou 730046, China.
Viruses. 2025 Jun 23;17(7):883. doi: 10.3390/v17070883.
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.
磷脂酶A2G16(PLA2G16)是磷脂酶A2家族的成员,可催化从磷脂酸生成溶血磷脂酸(LPA)和游离脂肪酸(FFA)。此前,发现PLA2G16是小RNA病毒的宿主因子。在此,我们发现口蹄疫病毒(FMDV)感染导致PLA2G16转录水平升高。我们在PK-15细胞中建立了PLA2G16过表达和敲低细胞系,以研究PLA2G16在FMDV感染中的潜在作用。我们的研究结果显示,在FMDV感染期间,过表达PLA2G16的细胞中磷酸化STAT1以及干扰素刺激因子ISG15和ISG56的水平升高。在过表达PLA2G16的细胞中,观察到p-STAT1的水平高于野生型细胞,且出现时间更早。后续研究表明,PLA2G16特异性促进针对FMDV的抗病毒先天免疫反应。宿主能够在过表达PLA2G16的细胞中检测到FMDV病毒核酸的早期释放,并触发干扰素信号通路。此外,我们发现过表达PLA2G16的细胞的上清液刺激产生更高水平的ISG56和磷酸化STAT1。这表明过表达PLA2G16的细胞在FMDV感染后可激活未感染细胞的先天免疫途径。