How Monocyte Chemotactic Protein-1 Mediates In Atherogenesis Because Of Human Cytomegalo-virus Infection

Objective: The incidence rate of ischemic cerebrovascular disease tend to increase every year,especially among young people.It's pressing to find its causes and promotion circumstances and then work on to prevention and cure this disease. Artherosclerosis is the main foundation of pathology in cerebral infarction. Increasing attention is being paid to the viral etiology of atherosclerosis (AS) for more and more scholars Since Fabricant inoculated Marekvirus to turkey and made it provoke atherosclerosis[33] , and Human cytomegalo-virus (HCMV) is thought to be the most possible etiological factor of atherosclerosis. We have proved that the active infection of Human cytomegalo-virus (HCMV) is relevant to atherosclerosis in ten years'study. However, we do not exactly know how infection of HCMV participates in the process of atherosclerosis. The main of this article is to investigate how monocyte chemotactic protein-1(MCP-1)mediates in atherogenesis because of HCMV infection.Method:1 The investigation subjects were 69 cases which were consistent with selecting qualification ,all of the cases conduct ultrasound of arteria carotid,HCMV-PP65 of peripheral blood leucocyte,MCP1. Compare the differences of HCMV-PP65,MCP1 in the patients with different kinds of plaques, further to compare the difference of MCP1 between PP65 positive and negative patients.2 Ultrasound examination method: Use color Doppler ultrasonograph of HDI ATL 5000 producted by American, with linear array detecting head, frequency of waves is 5～12MHZ.With dorsal position, detecte from originate of arteria carotis to earteria carotis interna when entered the skull.Examine both of the arteria carotis use consecutive T-sect,longitudinal plane 2D gray-scale and frequency spectrum ultrasonic examination by Doppler's method. Review and record the IMT,mainly observe whether exist atherosclerotic plaque or not, the position,size,resonance,surface characteristic of atherosclerotic plaque.3 Detect HCMV-PP65 antigen in peripheral blood leucocyte use the method of immunohistochemical; Assaying MCP1 in peripheral blood use the metod of biocatalyst connected immune adsorption double antibody sandwich.4 The various plaques were grouped into 6 types on the basis of the course of disease development, kinds of pathologic changes and Hennerici[32] classification. For the statistical convenience, the patients with soft and flat plaque were included into instable-plaque group, the patients with endometrial hyperplasia and hard plaque were classified into method according to the report and photograph.Results:1 HCMV-PP65 postive rate in plaque group is 56.00%, with 31.58% in no-plaque group. There is a significant difference between the HCMV-PP65 postive rate in plaque group and the one in no-plaque group (P<0.05).2 The cases are grouped into 3 types which are named instable-plaque group,stable-plaque group and no-plaque group. Different groups have different HCMV-PP65 postive rates:The rates in each group are 68.75%,33.33% and 31.58% ,respectively. The HCMV-PP65 postive rate in instable-plaque group is obviously higher than those of the other two groups(P<0.05).3 The average contents of MCP1 are 5.5819 ng/ml in HCMV-PP65 positive group and 3.7584 ng/ml in negtive one. There is a significant difference between the contents of the two groups (P<0.05).4 The average content of MCP1 in plaque group is 5.1522 ng/ml, with 3.3535 ng/ml in no-plaque group, and the level of MCP1 of the fomer is higher than that of the latter (P<0.05). The average content of MCP1 in instable-plaque group is 5.8754 ng/ml, with 3.8665 ng/ml in stable-plaque group, and the level of MCP1 of the fomer is also higher than that of the latter (P<0.05). The data suggest the expression of MCP-1 differs along with the type of plaques. 5 In the positive cases, the average content of MCP1 in plaque group is 6.1068 ng/ml, with 3.1325 ng/ml in no-plaque group, and the level of MCP1 of the fomer is higher than that of the latter (P<0.05). The average content of MCP1 in instable-plaque group is 6.6842 ng/ml, with 3.9897 ng/ml in stable-plaque group, and the level of MCP1 of the fomer is also higher than that of the latter (P<0.05). After infection of HCMV is activated , there is a positive correlation between the expression of MCP-1 and instability of plaque.Conclusions: 1 Activated infection of HCMV which plays an important role in atherogenesis is prone to increase the instability of plaques.2 Activated infection of HCMV can increase the expression of MCP-1.3 MCP-1 has positive correlate with HCMV and AS, and inflammatory reaction of infection of HCMV plays an important role in atherogenesis.