Atherosclerosis is a complex inflammatory disease process of the arterial vessels.¹ Chronic and acute infections have been implicated as risk factors that increase the risk of stroke, myocardial infarction (MI) and other vascular events. However, no single pathogen is likely to be responsible for elevated vascular risk.² More likely, the combined effect of long-term exposure to multiple pathogens, or ‘infectious burden’ (IB), is more relevant to the study of vascular disease and stroke. The role of infections in vascular disease may also extend to acute precipitants of vascular events. This article reviews the postulated mechanisms of infection-induced vascular damage, host determinants of infection-mediated vascular effects and clinical evidence linking individual and composite measures of IB and stroke risk, and also provides a review of recent research evaluating intervention strategies.

Pathogens as Risk Factors for Atherosclerosis
Chlamydia pneumoniae
Chlamydia pneumoniae is a common respiratory pathogen believed to be responsible for approximately 10% of non-hospital-acquired pneumonias.³ C. pneumoniae is one of the best-studied organisms believed to be associated with cardiovascular disease. Studies that have evaluated human samples of atherosclerotic lesions using electron microscopy, molecular DNA methods and immunostaining techniques have identified C. pneumoniae in coronary, carotid, aortic and popliteal plaque.⁴ The majority of these studies have identified pathogen DNA or antigen only; however, a few studies have isolated viable C. pneumoniae organisms.^5,6 C. pneumoniae has been identified in both early- and late-stage fibrous plaque and, in particular, in carotid and cerebral arterial vessels.^7–9

Herpesvirus Family
Herpesviruses were initially identified as potential causes of atherosclerosis in animal models, and they have been the target of investigations into the association of infectious agents and atherosclerosis since then.¹⁰ The most thoroughly investigated of the eight herpesvirus known to commonly infect humans are herpes simplex virus 1 (HSV1), HSV2 and cytomegalovirus (CMV). HSV1 infection has been associated with accelerated atheroma formation in apolipoprotein E-/- (apoE-/-) mice, with a reduction in progression when treated with antiviral therapies.¹¹ HSV1 DNA has been found in some but not all samples of carotid atherosclerotic lesions.^12,13 The recurrent outbreaks associated with HSV infection and high population prevalence of exposure have made it an interesting target for epidemiological study.¹¹ For CMV, evidence for involvement in vascular disease has been garnered from polymerase chain reaction (PCR) detection of CMV DNA in atherosclerotic lesions. For example, Hendrix et al. found CMV DNA in 90% of advanced atherosclerotic lesions compared with only 50% of control patients with no or minimal atherosclerosis.¹⁴ The complete CMV genome has been identified in asymptomatic individuals, indicating persistent latent stage within the host cells.^14,15 Additional evidence of CMV causing a vasculopathy is derived from the evidence of association of CMV and advanced progression of atherosclerosis and vasculopathy in hearttransplant recipients.¹⁶

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