Figure 5. Infection-induced stimulation of accelerated atherosclerosis by molecular mimicry. Molecular mimicry requires infection by a pathogen that possesses a molecule with significant homology to a host molecule. Following a host response initiated to this molecule, the response then presents as an auto-immune insult against those tissues with cross-reactive epitopes. Depicted here, conserved proteins such as bacterial HSPs (pink diamonds) and host HSPs (pink diamonds with cross) are exposed as a result of tissue damage and the host response to infection. Specific antibody directed toward bacterial HSPs would cross-react with human HSPs, setting in motion a localized auto-immune response. Indeed, cross-reactive antibodies to bacterial and host HSPs have been reported. The resulting inflammatory response could lead to endothelial cell damage, and ultimately, together with monocyte recruitment and the presence of elevated circulating lipids such as ox-LDL, to the acceleration of the atheroma.