EMCV VP2 通过 Caspase 依赖性凋亡降解 IFI16,以逃避 IFI16-STING 通路。

IF 4 3区 医学 Q2 VIROLOGY
Ruofei Feng, Dianyu Li, Zhenfang Yan, Xiangrong Li, Jingying Xie
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引用次数: 0

摘要

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依赖型I型干扰素(IFN-I)的产生和抗病毒免疫。然而,IFI16-STING 信号通路如何受 EMCV 感染调控仍未得到很好的阐明。本研究调查了 IFI16 与 EMCV 之间的相互作用。结果表明,EMCV 感染抑制了 IFI16 在 A549 细胞中的表达。这项研究揭示了 IFI16 在对抗 EMCV 中的积极作用。在筛选与 IFI16 结合的病毒蛋白时,我们发现 EMCV VP2 蛋白通过树突酶依赖的细胞凋亡途径导致 IFI16 蛋白降解,从而阻碍了 IFI16 介导的抗病毒反应。我们的研究揭示了 IFI16-STING 通路在 EMCV 感染过程中的抗病毒作用。重要的是,这项研究揭示了 VP2 抵消外来 DNA 激活的先天免疫信号的新机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
EMCV VP2 degrades IFI16 through Caspase-dependent apoptosis to evade IFI16-STING pathway.

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.

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来源期刊
Virology Journal
Virology Journal 医学-病毒学
CiteScore
7.40
自引率
2.10%
发文量
186
审稿时长
1 months
期刊介绍: Virology Journal is an open access, peer reviewed journal that considers articles on all aspects of virology, including research on the viruses of animals, plants and microbes. The journal welcomes basic research as well as pre-clinical and clinical studies of novel diagnostic tools, vaccines and anti-viral therapies. The Editorial policy of Virology Journal is to publish all research which is assessed by peer reviewers to be a coherent and sound addition to the scientific literature, and puts less emphasis on interest levels or perceived impact.
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