Chinese Medical Sciences Journal ›› 2024, Vol. 39 ›› Issue (1): 1-8.doi: 10.24920/004319

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Antiviral Effect of Extracellular Matrix Protein ABI3BP on Vesicular Stomatitis Virus and Its Mechanism: A Preliminary Study In Vitro

Xiang-Bo Meng1, 2, Mei-Hua Chen3, Nuo Xu1, 2, Tian-Qi Li1, 2, Shuai-Chen Li1, 2, Sun-Xin Zhou1, 2, Huan Chen4, *(), Tong Zhang1, *()   

  1. 1Department of Stomatology, the First Medical Center, Chinese People’s Liberation Army (PLA) General Hospital, Beijing 100853, China
    2Chinese PLA Medical School, Beijing 100853, China
    3State Key Laboratory of Toxicology and Medical Countermeasures, Beijing Institute of Pharmacology and Toxicology, Beijing 100850, China
    4Baodi Clinical College, Tianjin Medical University, Tianjin 301800, China
  • Received:2023-10-20 Accepted:2023-12-27 Published:2024-03-31 Online:2024-02-22
  • Contact: * Tong Zhang, E-mail: kqzhengji301@163.com;Huan Chen, E-mail: 1773524536@qq.com.

Objective To explore the influence of extracellular matrix protein ABI-interactor 3-binding protein (ABI3BP) on vesicular stomatitis virus (VSV) genome replication and innate immune signaling pathway.

Methods The small interfering RNA (siRNA) was transfected to knock down ABI3BP gene in human skin fibroblast BJ-5ta cells. VSV-green fluorescent protein (VSV-GFP)-infected cell model was established. The morphological changes and F-actin stress fiber formation were detected on ABI3BP knockdown cells by phalloidin immunofluorescence staining. The mRNA level of virus replication was detected by RT-qPCR in BJ-5ta cells after VSV-GFP infection; western blotting was performed to detect the changes in interferon regulatory factor 3 (IRF3) and TANK-binding kinase 1 (TBK1) phosphorylation levels.

Results The VSV-GFP-infected BJ-5ta cell model was successfully established. Efficient knockdown of ABI3BP in BJ-5ta cells was achieved. Phalloidin immunofluorescence staining revealed structural rearrangement of intracellular F-actin after ABI3BP gene knockdown. Compared with the control group, the gene copy number of VSV-GFP in ABI3BP knockdown cells increased by 2.2 - 3.5 times (P<0.01) and 2.2 - 4.0 times (P<0.01) respectively when infected with VSV of multiplicity of infection 0.1 and 1. The expression of viral protein significantly increased in ABI3BP knockdown cells after virus infection. The activation of type-I interferon pathway, as determined by phosphorylated IRF3 and phosphorylated TBK1, was significantly decreased in ABI3BP knockdown cells after VSV-GFP infection.

Conclusions Extracellular matrix protein ABI3BP plays an important role in maintaining the formation and rearrangement of actin structure. ABI3BP gene deletion promotes RNA virus replication, and ABI3BP is an important molecule that maintains the integrity of type I interferon pathway.

Key words: ABI-interactor 3-binding protein, extracellular matrix protein, actin, vesicular stomatitis virus, viral replication

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