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Comparative transcriptome reveals EphA2 and c-Fos as key factors driving enhanced replication in high-passage porcine deltacoronavirus strain

文献类型： 外文期刊

作者： Liu, Shiyu 1 ; Peng, Qi 4 ; Fan, Baochao 1 ; Zhang, Gege 1 ; He, Wenlong 1 ; Wang, Chuanhong 1 ; Xie, Jingyuan 1 ; Song, Xu 1 ; Yuan, Boshui 1 ; Guo, Rongli 1 ; Li, Jizong 1 ; Li, Bin 1 ;

作者机构： 1.Jiangsu Acad Agr Sci, Inst Vet Med,Key Lab Vet Biol Engn & Technol, Jiangsu Key Lab Food Qual & Safety,Minist Agr, State Key Lab Cultivat Base,Minist Sci & Technol, Nanjing 210014, Peoples R China

2.Nanjing Agr Univ, Coll Vet Med, Nanjing 210095, Jiangsu, Peoples R China

3.Yangzhou Univ, Jiangsu Coinnovat Ctr Prevent & Control Important, Yangzhou 225009, Peoples R China

4.Jiangxi Agr Univ, Inst Pathogen Microorganism, Nanchang 330045, Peoples R China

5.Jiangsu Univ, Sch Life Sci, Zhenjiang 212013, Peoples R China

6.Jiangsu Univ, Sch Food & Biol Engn, Zhenjiang 212013, Peoples R China

关键词： PDCoV; LLC-PK1; RNA-Seq; MAPK pathway; EphA2; C-Fos

期刊名称：VETERINARY MICROBIOLOGY （ 影响因子：2.4； 五年影响因子：2.6 ）

ISSN： 0378-1135

年卷期： 2024 年 297 卷

页码：

收录情况： SCI

摘要： Porcine deltacoronavirus (PDCoV), a cross-species transmissible enterovirus, frequently induces severe diarrhea and vomiting symptoms in piglets, which not only pose a significant menace to the global pig industry but also a potential public safety risk. In a previous study, we isolated a vaccine candidate, PDCoV CZ2020-P100, by passaging a parental PDCoV strain in vitro, exhibiting attenuated virulence and enhanced replication. However, the factors underlying these differences between primary and passaged strains remain unknown. In this study, we present the transcriptional landscapes of porcine kidney epithelial cells (LLC-PK1) cells infected with PDCoV CZ2020-P1 strain and P100 strain using the RNA-sequencing. We identified 105 differentially expressed genes (DEGs) in P1-infected cells and 295 DEGs in P100-infected cells. Enrichment analyses indicated that many DEGs showed enrichment in immune and inflammatory responses, with a more and higher upregulation of DEGs enriched in the P100-infected group. Notably, the DEGs were concentrated in the MAPK pathway within the P100-infected group, with significant upregulation in EphA2 and c-Fos. Knockdown of EphA2 and c-Fos reduced PDCoV infection and significantly impaired P100 replication compared to P1, suggesting a novel mechanism in which EphA2 and c-Fos are highly involved in passaged virus replication. Our findings illuminate the resemblances and distinctions in the gene expression patterns of host cells infected with P1 and P100, confirming that EphA2 and c-Fos play key roles in high-passage PDCoV replication. These results enhance our understanding of the changes in virulence and replication capacity during the process of passaging.

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