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Open Access 01-12-2024 | Research

EMCV VP2 degrades IFI16 through Caspase-dependent apoptosis to evade IFI16-STING pathway

Authors: Ruofei Feng, Dianyu Li, Zhenfang Yan, Xiangrong Li, Jingying Xie

Published in: Virology Journal | Issue 1/2024

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Abstract

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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Metadata
Title
EMCV VP2 degrades IFI16 through Caspase-dependent apoptosis to evade IFI16-STING pathway
Authors
Ruofei Feng
Dianyu Li
Zhenfang Yan
Xiangrong Li
Jingying Xie
Publication date
01-12-2024
Publisher
BioMed Central
Published in
Virology Journal / Issue 1/2024
Electronic ISSN: 1743-422X
DOI
https://doi.org/10.1186/s12985-024-02568-8

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