# Seneca valley virus VP4 protein regulates the transcription of different cytokines in vitro

**Authors:** Chaoliang Leng, Yu Ge, Mengfan Ruan, Wenxiao Zhao, Ximei Yang, Sainan Gao, Hongyue Zhai, Dandan Li, Dan Rao, Jianguo Dong

PMC · DOI: 10.3389/fvets.2025.1675546 · Frontiers in Veterinary Science · 2025-10-16

## TL;DR

This study shows how the VP4 protein from Seneca valley virus affects immune-related genes in cells, offering insights into virus behavior and vaccine development.

## Contribution

The study reveals the VP4 protein's specific regulation of cytokine transcription, providing new insights into SVV pathogenesis.

## Key findings

- Overexpression of VP4 significantly promotes IL-1α and IL-1β transcription at 24 and 36 hours.
- CCL-2 and CCL-5 transcription is significantly increased at 36 hours, while CCL-10 is increased only at 12 hours.
- TNF-α transcription is significantly inhibited at all three time points.

## Abstract

To understand the effect of Seneca valley virus (SVV) VP4 protein on innate immune factors, the VP4 gene was cloned into the pEGFP-C1 expression plasmid to construct the pEGFP-C1-VP4 recombinant plasmid. After the recombinant plasmid was transfected into 293 T cells, the cell fluid was collected 24 h after transfection for western blot assay to identify the correctness of VP4 protein expression. Cell culture medium was collected from un-transfected and transfected cells at three time points (12, 24, and 36 h). mRNA expression levels of cytokines (IL-1α, IL-1β, CCL-2, CCL-5, CXCL-10, and TNF-α) at three time points were detected by quantitative real-time PCR (qPCR) method, and relative quantitative analysis was performed by 2-ΔΔCt method. The results indicated that the expressed SVV VP4 protein exhibits good activity in vitro. Overexpression of the VP4 protein could significantly promote the transcription of IL-1α and IL-1β at 24 and 36 h. In addition, the transcription of CCL-2 and CCL-5 was also significantly promoted at 36 h, whereas the transcription of CCL-10 was significantly promoted only at 12 h. The TNF-α transcription was significantly inhibited at all the three time points. This study provides an important basis for the pathogenic mechanism of SVV and vaccine design in the future.

## Linked entities

- **Genes:** IL1A (interleukin 1 alpha) [NCBI Gene 3552], IL1B (interleukin 1 beta) [NCBI Gene 3553], CCL2 (C-C motif chemokine ligand 2) [NCBI Gene 6347], CCL5 (C-C motif chemokine ligand 5) [NCBI Gene 6352], CXCL10 (C-X-C motif chemokine ligand 10) [NCBI Gene 3627], TNF (tumor necrosis factor) [NCBI Gene 7124]
- **Proteins:** VP4 (minor core protein VP4)

## Full-text entities

- **Genes:** CCL5 (C-C motif chemokine ligand 5) [NCBI Gene 6352] {aka D17S136E, RANTES, SCYA5, SIS-delta, SISd, TCP228}, CXCL10 (C-X-C motif chemokine ligand 10) [NCBI Gene 3627] {aka C7, IFI10, INP10, IP-10, SCYB10, crg-2}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, CCL2 (C-C motif chemokine ligand 2) [NCBI Gene 6347] {aka GDCF-2, HC11, HSMCR30, MCAF, MCP-1, MCP1}, IL1A (interleukin 1 alpha) [NCBI Gene 3552] {aka IL-1 alpha, IL-1A, IL1, IL1-ALPHA, IL1F1}
- **Species:** Senecavirus A (no rank) [taxon 390157]
- **Cell lines:** 293 T — Homo sapiens (Human), Transformed cell line (CVCL_0063)

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12571611/full.md

## References

30 references — full list in the complete paper: https://tomesphere.com/paper/PMC12571611/full.md

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Source: https://tomesphere.com/paper/PMC12571611