Chronic infections and atherosclerosis/thrombosis

Abstract

An emerging pathophysiologic paradigm implicates chronic inflammation in the initiation, progression, and destabilization of atherosclerotic vascular disease. Various potential contributors to the inflammatory response in the vessel wall include atherogenic lipids, mechanical stress and injury, hypertension and angiotensin II, cigarette smoking, immune response to neoantigens, and chronic infections with viruses and or bacteria (Table 1). The potential link between chronic infection and atherosclerosis/thrombosis is under extensive investigation in several laboratories around the world. Although indirect evidence and experimental data tend to support this link, definitive proof is still lacking. If such a link is eventually proven to be causal in nature, it will provide a novel target for preventive and therapeutic strategies (anti-infective drugs, vaccines, etc.) against a common disease that is the leading killer of people in Western nations. Results of ongoing, large-scale clinical trials are eagerly awaited.