Evidence map›Paper›PMID 38822277›Full record

ArticleCellular & molecular biology letters2024

ZBP1 inhibits the replication of Senecavirus A by enhancing NF-κB signaling pathway mediated antiviral response in porcine alveolar macrophage 3D4/21 cells.

Huizi Li, Tingting Zheng, Ming Chen, Xiaoling Lei, Shuo Li, Xijiao Chen, Shishi Wang, Zhangyong Ning

Abstract read
In one paragraph

Article in Cellular & molecular biology letters, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Huizi Li *College of Veterinary Medicine, South China Agricultural University, Guangzhou, 510642, China.
Tingting Zheng *College of Veterinary Medicine, South China Agricultural University, Guangzhou, 510642, China.
Ming ChenCollege of Veterinary Medicine, South China Agricultural University, Guangzhou, 510642, China.
Xiaoling LeiCollege of Veterinary Medicine, South China Agricultural University, Guangzhou, 510642, China.
Shuo LiCollege of Veterinary Medicine, South China Agricultural University, Guangzhou, 510642, China.
Xijiao ChenCollege of Veterinary Medicine, South China Agricultural University, Guangzhou, 510642, China.
Shishi WangCollege of Veterinary Medicine, South China Agricultural University, Guangzhou, 510642, China.
Zhangyong NingCollege of Veterinary Medicine, South China Agricultural University, Guangzhou, 510642, China. ningzhyong@scau.edu.cn.ORCID http://orcid.org/0000-0002-0591-8588

Funding

Project of Swine Innovation Team in Guangdong Modern Agricultural Research System 2020KJ126Start-up Research Project of Maoming Laboratory 2021TDQD002
6 · The paper itself

Abstract

backgroundSenecavirus A (SVA) caused porcine idiopathic vesicular disease (PIVD) showing worldwide spread with economic losses in swine industry. Although some progress has been made on host factors regulating the replication of SVA, the role of Z-DNA binding protein 1 (ZBP1) remains unclear.

methodsThe expression of ZBP1 in SVA-infected 3D/421 cells was analyzed by quantitative real-time PCR (qRT-PCR) and western blot. Western blot and qRT-PCR were used to detect the effects of over and interference expression of ZBP1 on SVA VP2 gene and protein. Viral growth curves were prepared to measure the viral proliferation. The effect on type I interferons (IFNs), interferon-stimulated genes (ISGs), and pro-inflammatory cytokines in SVA infection was analyzed by qRT-PCR. Western blot was used to analysis the effect of ZBP1 on NF-κB signaling pathway and inhibitor are used to confirm.

resultsZBP1 is shown to inhibit the replication of SVA by enhancing NF-κB signaling pathway mediated antiviral response. SVA infection significantly up-regulated the expression of ZBP1 in 3D4/21 cells. Infection of cells with overexpression of ZBP1 showed that the replication of SVA was inhibited with the enhanced expression of IFNs (IFN-α, IFN-β), ISGs (ISG15, PKR, and IFIT1) and pro-inflammatory cytokines (IL-6, IL-8, and TNF-α), while, infected-cells with interference expression of ZBP1 showed opposite effects. Further results showed that antiviral effect of ZBP1 is achieved by activation the NF-κB signaling pathway and specific inhibitor of NF-κB also confirmed this.

conclusionsZBP1 is an important host antiviral factor in SVA infection and indicates that ZBP1 may be a novel target against SVA.

Indexed as

Macrophages, AlveolarNF-kappa BPicornaviridaeSignal TransductionVirus ReplicationAnimalsCell LineCytokinesRNA-Binding ProteinsSwineCytokinesNF-kappa BRNA-Binding ProteinsNF-κBSVAZBP1

Identifiers

PMID38822277
PMCPMC11140869

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.