FMDV 3A cooperates with PDCD10 to promote FMDV replication by inhibiting VISA-mediated innate immunity

Foot-and-mouth disease virus (FMDV) is a pathogen that causes a highly contagious and destructive foot-and-mouth disease in animals with cloven hooves. Although the 3A protein of FMDV is involved in viral replication and host tropism, its function remains unclear. PDCD10 plays critical roles in normal cardiovascular development, cell proliferation, and normal structure and assembly of the Golgi complex. The present study showed that PDCD10 expression was slightly increased by virus infection, while PDCD10 promoted FMDV replication. Our results also demonstrated that PDCD10 inhibited Sendai virus-induced interferon beta (IFN-β) production through interaction with virus-induced signaling adaptor (VISA). PDCD10 also disrupted VISA-IRF3 complex formation to impair IFN-β production induced by RNA virus. The FMDV 3A protein bound with PDCD10 to synergistically promote FMDV replication. This study helped to reveal the potential mechanism of FMDV 3A protein and PDCD10 impact on viral replication.

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Publication Details

Journal
Journal of Virology
Published
2025-11-26
DOI
https://doi.org/10.1128/jvi.00657-25
Primary Topic
Animal Disease Management and Epidemiology
Type
article
Field-Weighted Citation Impact
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article

FMDV 3A cooperates with PDCD10 to promote FMDV replication by inhibiting VISA-mediated innate immunity

Zixiang Zhu, Xiaofeng Nian, ZongBo Zeng, Xinting Ma et al.
Journal of Virology
Animal Disease Management and Epidemiology
article

FMDV 3A cooperates with PDCD10 to promote FMDV replication by inhibiting VISA-mediated innate immunity

Zixiang Zhu, Xiaofeng Nian, ZongBo Zeng, Xinting Ma, Fan Yang, Zhikuan Luo, Medvedev Ma, Yi‐Gang Xu, Qian Li, Li Li, Haixue Zheng, Xiaofen Shang, Jingjing Pei, Hongbin Yan, Weijun Cao, Bo Du
article en

Abstract

Foot-and-mouth disease virus (FMDV) is a pathogen that causes a highly contagious and destructive foot-and-mouth disease in animals with cloven hooves. Although the 3A protein of FMDV is involved in viral replication and host tropism, its function remains unclear. PDCD10 plays critical roles in normal cardiovascular development, cell proliferation, and normal structure and assembly of the Golgi complex. The present study showed that PDCD10 expression was slightly increased by virus infection, while PDCD10 promoted FMDV replication. Our results also demonstrated that PDCD10 inhibited Sendai virus-induced interferon beta (IFN-β) production through interaction with virus-induced signaling adaptor (VISA). PDCD10 also disrupted VISA-IRF3 complex formation to impair IFN-β production induced by RNA virus. The FMDV 3A protein bound with PDCD10 to synergistically promote FMDV replication. This study helped to reveal the potential mechanism of FMDV 3A protein and PDCD10 impact on viral replication.

Journal of VirologyVol. 99(12)
Northwest Minzu University (CN), Zhejiang A & F University (CN), Minzu University of China (CN), Gansu Agricultural University (CN), Northeast Agricultural University (CN), Lanzhou Veterinary Research Institute (CN), Zhejiang University of Technology (CN)
Openalex Percentile: Top 53%
Animal Disease Management and Epidemiology
DOIOpen Access PDFOpenAlex
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