巨细胞病毒感染与粘附分子-1基因转录水平的实验研究

目的研宄人巨细胞病毒(human cytomegalovirus,HCMV)感染人胚肺成纤维细胞(human embryonic lung,HEL)后粘附分子-1(ICAM-1)在基因转录水平的表达,探讨HCMV感染的发病机制.方法采用RT-PCR技术研究细胞ICAM-1-1在基因转录水平的表达.结果感染巨细胞病毒后ICAM-1的表达上调,而UV灭活的CMV不能诱导ICAM-1的上调,中药金叶败毒制荆与更昔洛韦(Ganciclovir,GCv)不能阻止病毒诱导的ICAM-1的上调.MEK特异性抑制子PD98059可加强ICAM-1的上调作用.结论细胞ICAM-1-1在转录水平的上调可能是感染病毒的直接作用,MEK特异性抑制子PD98059加强ICAM-1上调作用.

Experimental study on cytomegalovirus - induced ICAM - 1 mRNA in cultured human fibroblasts

Objective: To study the expression of intercellular adhesion molecule-1 in UV-inactivated virus, human Cytomegalovirus, and PD98059 and Jinyebaidu on human cytomegalovirus-infected fibroblasts, to determine the molecular mechanism of intercellular adhesion molecule-1 gene expression. Methods:The expression of ICAM-1 in human cytomegalovirus-infected fibroblasts and uninfected were evaluated by RT-PCR. Results: Our results indicate that intercellular adhesion molecule-1 expression was increased in human cytomegalovirus-infected fibroblasts compared with uninfected fibroblasts; Jinyebaidu did not suppress human cytomegalovirus induced upregulation of intercellular adhesion molecule-1 just like GCV. Interestingly, PD98059, a specific inhibitor of MEK enhanced HCMV-induced upregulation of ICAM-1 to some extent. Conclusion: The results suggest that upregulation of intercellular adhesion molecule-1 is the direct virus effect. PD98059 enhanced the upregulation of intercellular adhesion molecule-1.