Key Laboratory of Biotechnology and Bioengineering of State Ethnic Biomedical Research Center, Northwest Minzu University, Lanzhou, China.
Engineering Research Center of Key Technology and Industrialization of Cell-based Vaccine, Ministry of Education, Biomedical Research Center, Northwest Minzu University, Lanzhou, China.
Virol J. 2024 Nov 18;21(1):296. doi: 10.1186/s12985-024-02568-8.
Interferon (IFN)-γ inducible protein 16 (IFI16), a key DNA sensor, triggers downstream STING-dependent type I interferon (IFN-I) production and antiviral immunity. However, how the IFI16-STING signaling pathway is regulated by EMCV infection is still not well elucidated. In this study, we investigated the interaction between IFI16 and EMCV. Results indicated EMCV infection suppressed IFI16 expression in A549 cells. This study reveals that IFI16 plays an active role in combating EMCV. Screening viral proteins in conjunction with IFI16, we found that the EMCV VP2 protein hinders the antiviral response mediated by IFI16 by causing degradation of the IFI16 protein via the caspase-dependent apoptosis pathway. Our study communicates the antiviral role of the IFI16-STING pathway during EMCV infection. Importantly, this study unveils the novel mechanism by which VP2 counteracts the innate immune signaling activated by foreign DNA.
干扰素（IFN）-γ诱导蛋白 16（IFI16）是一种关键的 DNA 传感器，可触发下游 STING 依赖性 I 型干扰素（IFN-I）的产生和抗病毒免疫。然而，IFI16-STING 信号通路如何被 EMCV 感染调控仍不清楚。在这项研究中，我们研究了 IFI16 和 EMCV 之间的相互作用。结果表明，EMCV 感染抑制了 A549 细胞中的 IFI16 表达。这项研究揭示了 IFI16 在对抗 EMCV 中发挥着积极的作用。通过与 IFI16 联合筛选病毒蛋白，我们发现 EMCV VP2 蛋白通过 caspase 依赖性细胞凋亡途径导致 IFI16 蛋白降解，从而阻碍 IFI16 介导的抗病毒反应。我们的研究在 EMCV 感染过程中传达了 IFI16-STING 通路的抗病毒作用。重要的是，这项研究揭示了 VP2 拮抗外来 DNA 激活的先天免疫信号的新机制。
