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The inflammation hypothesis of atherosclerosis postulates that the crucial events involved in the initiation and progression of the lesion are represented mainly by inflammatory and fibroproliferative processes triggered by cytokines and growth factors.1 However, one of the most interesting developments in recent years has been the idea that infective agents may induce a pro-inflammatory effect and have a crucial role in atherothrombosis.1 In addition, at the beginning of the 1970s, the monoclonal hypothesis was first proposed, suggesting a potential role for viral infection in the atherosclerotic process.2 In particular, this theory proposed that a mutation or a viral agent may represent events able to transform a single smooth muscle cell into the progenitor of a proliferative clone, introducing the concept that the plaque may be considered a monoclonal benign neoplasm. Since then, many additional results have shown an association between infectious agents and the atherosclerotic process, although other studies have produced contrary results.1 Thus, the role of infection in the pathogenesis of this disease remains controversial. In particular, very few data on the relation …