Cytomegalovirus genome and the immediate-early antigen in cells of different layers of human aorta

A number of data suggest that reactivation of cytomegalovirus (CMV) latent in arterial wall cells may contribute to atherogenesis; however, there is n o direct evidence available. To address this issue, we have examined, using in situ hybridization or immunohistochemical staining, the frequency of oc currence of cells containing viral genome and of those expressing the IE 70 viral antigen in the endothelial layer and in deeper layers of human aorta s with or without visible atherosclerotic lesions. Using endothelial cell c ultures or tissue endothelial preparations, we found CMV-hybridizing endoth elial cells in 6 of 8 grossly normal aortas and in 16 of 18 lesioned aortas . Antigen-positive endothelial cells were detected in 1 of 5 grossly normal vessels and in 6 of 7 lesioned vessels. Infected endothelial cells were ab undant in areas adjacent to orifices of intercostal arteries of grossly nor mal aortas and in fatty spots of lesioned aortas, but no infected endotheli al cells were observed in most plaques examined. In paraffin sections of gr ossly normal vessels, we detected CMV genome in cells adjacent to lumen and in cells randomly scattered through subendothelial intima and the media; h owever, no immunoreactive viral protein was found in the same tissue sample s. In sections of lesioned vessels, clusters of CMV-hybridizing cells were found in the media in addition to infected cells randomly scattered through the intima and the media. In these samples of lesioned vessels, viral anti gen was detected in cells adjacent to lumen and in cells clustered at the i ntima/media border. We found antigen-positive cells in grossly normal areas of lesioned aortas and in fatty lesions, but not in plaques of the same ve ssels. The data suggest that accumulation of the immediate-early CMV antige n in cells of endothelial layer and development of antigen-positive cell cl usters in deeper layers of vascular wall accompany early atherogenic events in human aorta.