Herpes simplex virus (HSV), the viral agent causing human genital herpes, recurs easily and poses significant harm to patients, while also being associated with atherosclerosis (AS). Currently, no effective therapy or vaccine exists to combat HSV. Previous studies have demonstrated the presence of HSV and its DNA in AS-diseased tissue, yet the precise pathogenesis of HSV involvement remains unclear. To investigate the genetic mechanism of HSV-induced vascular endothelial injury and AS, a type of human umbilical vein endothelial cells (ECV-304 cells) cultured in vitro were infected with herpes simplex virus type 2 (HSV-2). The effect of HSV-2 on differential gene expression in ECV304 cells was investigated by gene microarray technology during the early stages of infection. The results revealed a total of 462 differentially expressed genes, with 318 genes exhibiting up-regulated expression and 144 genes showing down-regulated expression. Furthermore, bioinformatics analysis revealed that all 462 differentially expressed genes were implicated in 237 distinct biological processes. Notably, 79 of these biological processes demonstrated statistically significant differences (P < 0.05), encompassing critical functions such as protein synthesis, ribosome biogenesis and assembly, as well as DNA and mRNA metabolism. Our findings have unveiled the differentially expressed genes of HSV-2 in ECV304 cells during infection, offering crucial insights into the pathogenic mechanisms underlying HSV-2 invasion of endothelial cells and the pathobiology of AS.
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