The inability of traditional risk factors such as hypercholesterolemia, hypertension, and smoking to explain the incidence of atherosclerosis (AT) in about 50% of the cases prompted a search for additional putative risk factors involved in the development of the disease. Infectious agents have long been suspected to initiate/contribute to the process of AT. It has also been suggested that inflammation, either related to infectious agents or independent from infection, may mediate the atherogenic process [1, 2].