The role of host protein RBM8A in the replication of pseudorabies virus
10.16303/j.cnki.1005-4545.2025.10.05
- VernacularTitle:宿主蛋白RBM8A对猪伪狂犬病病毒复制的作用
- Author:
Xiangqi QIU
1
;
Jingyu SUN
1
;
Jianhang HE
1
;
Xing YANG
1
;
Xiuwen YANG
1
;
Guoqing ZHUANG
1
;
Aijun SUN
1
Author Information
1. 河南农业大学动物医学院国家动物免疫学国际联合研究中心,河南 郑州 450046
- Publication Type:Journal Article
- Keywords:
RBM8A;
pseudorabies virus;
antiviral;
replication;
proliferation curve
- From:
Chinese Journal of Veterinary Science
2025;45(10):2126-2132
- CountryChina
- Language:Chinese
-
Abstract:
RNA binding motif protein 8A(RBM8A)is an RNA binding protein,which is mainly in-volved in translation and cell cycle regulation.In addition,RBM8A is a core factor of the exon-junc-tion complex(EJC),which is highly expressed in cells,especially in cancer cells,and abnormally expressed in cytoplasm and nucleus.Studies have shown that RBM8A plays a key regulatory role in the replication process of some viruses,such as Flaviviridae viruses.Therefore,whether RBM8A is involved in the replication of pseudorabies virus(PRV)is unknown.Therefore,this study proved whether RBM8A is involved in the replication of PRV.In order to study the effect of RBM8A pro-tein on PRV replication,the eukaryotic expression plasmid pCAGGS-HA-RBM8A was designed and constructed to express RBM8A,and sh-RBM8A was simultaneously designed and constructed to overexpress and inhibit RBM8A.qRT-PCR and Western blot were used to detect the effect of RBM8A on PRV replication.At the same time,PRV-GB standard plasmid was constructed to make PRV proliferation standard curve.After overexpression and inhibition of RBM8A,DNA was ex-tracted.Virus copy number was calculated by qRT-PCR to further detect the effect of RBM8A on PRV replication.The results showed that overexpression of RBM8A inhibited PRV replication and decreased the copy number of the virus,while overexpression of shRBM8A promoted PRV replication and increased the copy number of the virus.This study shows that RBM8A can inhibit PRV replication,which provides reference for the functional study of RBM8A and lays a founda-tion for the mechanism of anti-PRV replication.
