Possible role of viruses in atherosclerosis

Relative to the role of viruses in the pathogenesis of atherosclerosis a number of questions remain to be answered. Being ubiquitous, are the herpesvirus infections the norm or a diseased state in humans and animals? In all cases studied, including MDV induced atherosclerosis, direct isolation of viruses from arterial tissues has not been successful. Are herpesviruses always latent or dormant in vascular tissues? What is the relationship between provirus and disease development? Are they setting the stage for the pathogenic process triggered by certain environmental factors? Is hypercholesterolemia to trigger the development of atherosclerosis in the presence of proviruses? Is the reactivated and infectious virus the injuring agent that initiates atherogenesis? Or, are the proviral genes activated to transform arterial cells? In the latter case, are these proviral genes equivalent to "proto-atherogenes"? Hopefully, further study on Japanese quail will help clarify many of these questions.