Transcriptomics analysis of echovirus type 11 infected RD cells
10.3760/cma.j.cn-112866-20210719-00130
- VernacularTitle:埃可病毒11型感染RD细胞的转录组学分析及PLK1对其感染影响的初步探究
- Author:
Guoyan ZHANG
1
;
Jichen LI
;
Keyi ZHANG
;
Qiang SUN
;
Yong ZHANG
;
Guizhen WU
Author Information
1. 中国疾病预防控制中心病毒病预防控制所 国家卫生健康委员会生物安全重点实验室 国家卫生健康委员会医学病毒与病毒病重点实验室 世界卫生组织西太平洋区脊髓灰质炎参比实验室，北京 102206
- Keywords:
Echovirus 11;
RNA-Seq;
PLK1;
Differentially expressed genes;
Host factor
- From:
Chinese Journal of Experimental and Clinical Virology
2021;35(6):605-611
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the transcriptional changes of host factors in human rhabdomyosarcoma cells (RD) infected with echovirus 11 (E11), and to preliminarily understand the effect of polo like kinase 1(PLK1)on E11 replication and possible molecular mechanism.Methods:Transcriptome sequencing (RNA SEQ) was used to analyze the differentially expressed genes between E11 infected RD cells group and RD cell control group. Gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) was used to enrich and analyze significantly differentially expressed genes. The expression situation of the representative differentially expressed genes were validated by quantitative real-time polymerase chain reaction (qRT-PCR), and the effect of PLK1 inhibition on E11 replication was preliminarily explored.Results:A total of 3 726 differentially expressed genes were identified in RD cells infected with E11, and 484 differentially expressed genes were found in the infected group (0 h, 12 h, 24 h and 48 h after infection). These differentially expressed genes were mainly enriched in the immune response, intracellular signal transduction, transcription factor activity, sequence-specific DNA binding, protein kinase activity, nuclear and membrane components, and PI3K-Akt signaling pathway. qPCR was used to verify the expression of six target genes (CXCL14, IFITM1, OAS1, SAMD9, MX1 and PLK1), which were consistent with result of RNA-Seq. The expression of CXCL14, IFITM1, OAS1, SAMD9, and MX1 were up-regulated by 1.2-104.97 times, and the expression of PLK1 was down regulated by 1-5.79 times. Inhibition of PLK1 increased E11 replication.Conclusions:Inflammatory response, PI3K-Akt, MAPK and other pathways may play an important role in the antiviral immune process of E11 infection. In addition, host factor PLK1 may play a key role in E11 infection by regulating the cell cycle.
