| Background:Atherosclerosis is the major cause of cardiovascular disease, a major lethal disease to human health. There are increasing evidences to support a role for infection contributing to atherosclerosis, to date, several infections agents causing persistent or latent chronic infections have been identified as possible etiologic cofactors. Especially, since Fabricant used Herpes virus induced atherosclerosis in chicken , there are mo:re and more seroepidemiologic evidences linking herpesvirus infection and atherosclerosis, studies in human beings indicate that human cytomegalovirus are involved in vascular disease such as atherosclerosis ,restenosis ,and transplantation arteriosclerosis. In vitro and in vivo studies provide interesting data of possible mechanisms playing a role in the pathogenesis of atherosclerosis.CMV infection or reactivation from latency in vascular cells have been shown to contribute to atherosclerosis several lines of evidence support this concept: in studies on human-derived tissues, CMV-DNA sequence were detected in the wall of atherosclerotic vessels and accelerated coronary atherosclerosis is more common in cardiac transplant patients exposure.Human cytomegalovirus (HCMV), a member of the Herpesvirus family, is one of the important pathogen to human being; the association between HCMV and atherosclerosis is based on seroepidemiologic studies. And it has been suggested that active HCMV infection could participate in the cascade of events leading to the atherosclerosis The demonstration of HCMV DNA in atherosclerotic plaque tissue, and multiple mechanistic studies indicating that infection of vascular wall cells(SMCs,ECs) produces cellular changes that would be conducive to the development of atherosclerosis, but whether HCMV infection plays a causative role is yet to be elucidated. So the biological effects of endothelial cells and smooth muscle cells after human cytomegalovirus infection should be further studies, the relationship between HCMV infection and AS should also be further studied, the study results will be useful to disclose mechanism of atherosclerosis.Purposes:The purposes of present study are:(1) To determine whether HCMV infection induced endothelial cells injure in vitro, especially, the change in functions and metabolism.(2) To study how does HCMV regulate LRP and IE gene, L gene , and to study the antiviral activity of GCV and ASON on SMCs after HCMV infection.(3) To further explore the relationship between HCMV infection and atherosclerosis in CHD patients and the putative mechanism.Methods:We used HCMV ADI 69 strain infected ECs and SMCs in vitro, and builted the model of HCMV infection to cell.1 To the model of ECs infection: the changes in metabolism and function of ECs after infection were observed; the cytophathic effect of ECs were studied by light microscope electron microscope, the apoptosis of ECs were analysed with Flow Cytometry ,the ATPase activity was detected by chemical methods.2 To the model of SMCs infection: the low density lipoprotein receptor-related protein(LRP) mRNA expression in smooth muscle cells was determined by reverse transcriptase-polymerase chain reaction (RT-PCR), and was normalized with B -actin mRNA , and the LRP protein expression in SMC was determined by cell enzyme linked immunosorbent assay total cholesterol(TC) and triglyceride(TG ) of the cell was extracted and determined . And in the mean time we used antisense phosphorothioate deoxyoligonucleotid (ASON) and ganciclovir (GCV) acted with infected SMC at different time.3 To 119 patients of CHD: the nucleic acid quantity of HCMV in serum of CHD patients were detected by Fluorogenic quantitative PCR (FQ-PCR), the HCMV IgG and IgM antibodies were detected by ELISA, and the levels of serum AEAC, hs-CRP, TNF, ET, were also analyzed simultaneously.Results:1. HCMV could replicate in ECs in vitro, the virus titer and HCMV DNA copies changed with the infection time, and at 48h after infection the titer of HCMV reached peak, and the c...
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