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Porcine Epidemic Diarrhea Virus (PEDV) ORF3 Enhances Viral Proliferation by Inhibiting Apoptosis of Infected Cells

文献类型： 外文期刊

作者： Si, Fusheng 1 ; Hu, Xiaoxia 1 ; Wang, Chenyang 1 ; Chen, Bingqing 1 ; Wang, Ruiyang 1 ; Dong, Shijuan 1 ; Yu, Ruisong; 1 ;

作者机构： 1.Shanghai Acad Agr Sci, Inst Anim Sci & Vet Med, Shanghai Key Lab Agr Genet & Breeding, Shanghai 201106, Peoples R China

2.Shanghai Engn Res Ctr Breeding Pig, Shanghai 201106, Peoples R China

3.Shanghai Ocean Univ, Natl Demonstrat Ctr Expt Fisheries Sci Educ, Shanghai 201306, Peoples R China

关键词： PEDV; the role of ORF3; proliferation; apoptosis; cells

期刊名称：VIRUSES-BASEL （ 影响因子：5.048； 五年影响因子：5.127 ）

ISSN：

年卷期： 2020 年 12 卷 2 期

页码：

收录情况： SCI

摘要： The genomes of coronaviruses carry accessory genes known to be associated with viral virulence. The single accessory gene of porcine epidemic diarrhea virus (PEDV), ORF3, is dispensable for virus replication in vitro, while viral mutants carrying ORF3 truncations exhibit an attenuated phenotype of which the underlying mechanism is unknown. Here, we studied the effect of ORF3 deletion on the proliferation of PEDV in Vero cells. To this end, four recombinant porcine epidemic diarrhea viruses (PEDVs) were rescued using targeted RNA recombination, three carrying the full-length ORF3 gene from different PEDV strains, and one from which the ORF3 gene had been deleted entirely. Our results showed that PEDVs with intact or naturally truncated ORF3 replicated to significantly higher titers than PEDV without an ORF3. Further characterization revealed that the extent of apoptosis induced by PEDV infection was significantly lower with the viruses carrying an intact or C-terminally truncated ORF3 than with the virus lacking ORF3, indicating that the ORF3 protein as well as its truncated form interfered with the apoptosis process. Collectively, we conclude that PEDV ORF3 protein promotes virus proliferation by inhibiting cell apoptosis caused by virus infection. Our findings provide important insight into the role of ORF3 protein in the pathogenicity of PEDV.

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