MCMV infection increases early T-lymphocyte influx in atherosclerotic lesions in apoE knockout mice.

BACKGROUND: Multiple epidemiological studies have suggested that cytomegalovirus (CMV) infection is associated with atherosclerotic disease. However, conclusive proof that the virus is directly related to the progression of the disease is still lacking.
OBJECTIVES: The goal of this study was to investigate whether MCMV is able to exacerbate the atherosclerotic process in atherosclerosis-susceptible mice. STUDY
DESIGN: apoE knockout mice kept on a chow diet were sacrificed at both 2 and 20 weeks post infection (p.i.). C57Bl/6J mice fed an atherogenic diet were sacrificed at 2 weeks p.i. Lesion area, lesion composition (endothelial cells and smooth muscle cells) and inflammatory influx (T-lymphocytes and macrophages) in lesions were determined. The former one was determined by means of a microscope coupled to a computer-assisted morphometry system. The latter ones were scored after immunohistochemical staining.
RESULTS: In the chronic phase of the infection mean lesion size was significantly increased after MCMV infection in the apoE knockout mice. This increase could to a large extent be attributed to a significant increase in type V lesion area after MCMV infection. Also, a significant increase in T-lymphocyte influx was observed in the acute phase of the infection in lesions from apoE knockout mice after MCMV infection while this effect was absent in C57Bl/6J mice. After MCMV infection no increase was observed in macrophage, smooth muscle cell and endothelial cell number in lesions from both mice strains.
CONCLUSIONS: MCMV infection may exacerbate the atherosclerotic process in apoE knockout mice by means of an acute lymphocytic inflammatory response. In contrast to the MCMV induced effect in apoE knockout mice, MCMV infection did not increase the influx of T-lymphocytes in atherosclerotic lesions of C57Bl/6J mice.