A RNA-seq-based study on differentially expressed genes related to the Inner Mongolia EV71 C33λ strain that invades Vero cells

Abstract

Enterovirus 71 (EV71) is a significant causative agent of hand, foot and mouth disease (HFMD). However, the precise mechanism by which EV71 infection leads to alterations in the immune response remain elusive. To address this knowledge gap, we conducted a study where we introduced the Inner Mongolia EV71 C33λ strain into Vero cells, derived from African green monkey kidney cells. Subsequently, we performed RNA sequencing (RNA-Seq) to investigate the changes in the transcriptome of these infected Vero cells. Our primary objective was to establish a foundational understanding that could inform future research on EV71-associated immune factors. In our study, we identified a total of 942 differentially expressed genes (DEGs) in Vero cells infected with Enterovirus 71 (EV71), with 568 gene exhibiting increased expression and 374 gene showing decreased expression. To elucidate the functional implications of these DEGs, we conducted a comprehensive functional enrichment analysis using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. This analysis revealed three genes that were significantly upregulated, which we subsequently validated using reverse transcription polymerase chain reaction technology (RT-qPCR). The RT-qPCR results were in strong agreement with our RNA-Seq data, confirming the reliability of our findings. This study represents the pioneering RNA-Seq analysis that delves into the cellular response of Vero cells to EV71 infection. Our results not only provide a foundational understanding of the molecular changes induced by EV71 but also offer crucial insights into the mechanisms by which EV71 modulates the host immune system. These insights are pivotal for future research endeavors aimed at developing effective therapeutic strategies against EV71 and related pathogens, as well as for understanding the broader implications of viral infections on host immunity.