Abstract: Objective Atherosclerosis plays an important role in the brain stroke. Cytomegalovirus(CMV) infection has been associated with atherosclerotic process. The goal of this study was to investigate whether murine cytomegalovirus(MCMV) infection is able to exacerbate the atherosclerotic process in atherosclerosis-susceptible mice. Methods The apolipoprotein E knockout(apoE-/-) mice kept on high fat feed were given low dosage of MCMV to mimic the latent stage of CMV infection in human. At 14. 18 and 24 weeks post infection, the area, number and type of atherosclerotic lesion and the intima/median ratio(I/M) were measured on aorta. The results were determined by means of a microscope coupled to a computer-assisted morphometry system. And the level of lectin-like ox-LDL receptor-1(LOX-1) mRNA in the arterial wall was measured by real-time PCR. The mechanism of MCMV infection on AS formation was investigated. Results In the chronic phase of the infection the area of lesion was significantly increased after MCMV infection in the apoE-/- mice. But with the increase of post-infection period, the role of MCMV on atherosclerosis reduced gradually. MCMV gB mRNA was not amplified by real-time PCR from the arterial wall. The specific IgG antibody level of MCMV in blood plasma and the content of virus DNA in salivary gland were not correlated with atherosclerotic lesions. At 14 weeks post infection, LOX-1 mRNA in arterial wall increased significantly in MCMV infected group. Conclusion MCMV may aggravate the atherosclerotic lesion in apoE-/- mice in the chronic phase of infection, and promote more severe type of atherosclerotic lesions. But it might not be the direct effects of MCMV on the local lesion of atherosclerosis. The increased expression of LOX-1 in arterial wall may be the mechanism through which MCMV aggravate the atherosclerosis.

Key words: murine cytomegalovirus, atherosclerosis, apolipoproteinE knockout mice, lectin ike ox DL receptor-1