Microbes have been proposed as inciting agents of tissue injury and inflamm
ation, both of which underlie the pathogenesis of atherosclerosis. Viruses,
including the herpes simplex virus and cytomegalovirus, as well as bacteri
a such as Chlamydia pneumoniae, have been Implicated in the process. In vit
ro, these agents promote a proinflammatory and a procoagulant phenotype in
vascular cells. Viruses augment cell accumulation through alterations of ap
optosis. Infectious agents may play a role in pathogenesis of atheroscleros
is by triggering an autoimmune response due to microbial molecular mimicry.
It is unlikely that a single agent is the sole cause or modulator of this
heterogeneous disease. Contradictory epidemiological studies may be reconci
led with a new construct suggesting that multiple pathogens infecting an in
dividual in aggregate may promote an inflammatory and procoagulant environm
ent that underlies the pathogenesis of atherosclerosis.