1998
DOI: 10.3109/15419069809005597
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Early Atherosclerotic Plaques in the Aorta Following Cytomegalovirus Infection of Mice

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Cited by 51 publications
(37 citation statements)
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“…Long-lasting hypercholesterolemia might, as shown in this report, mediate such defects in cellular immunity and therefore favor development of immunopathologic disease. Importantly, infection with herpesviruses (52,58) and acute LCMV infection, as shown here, can further alter cholesterol metabolism. Thus, self-perpetuating immunopathologic disease circuits may develop when chronic hypercholesterolemia-mediated immunosuppression impairs the usually well-balanced host-pathogen equilibrium.…”
Section: Discussionmentioning
confidence: 56%
See 1 more Smart Citation
“…Long-lasting hypercholesterolemia might, as shown in this report, mediate such defects in cellular immunity and therefore favor development of immunopathologic disease. Importantly, infection with herpesviruses (52,58) and acute LCMV infection, as shown here, can further alter cholesterol metabolism. Thus, self-perpetuating immunopathologic disease circuits may develop when chronic hypercholesterolemia-mediated immunosuppression impairs the usually well-balanced host-pathogen equilibrium.…”
Section: Discussionmentioning
confidence: 56%
“…Furthermore, it is striking that CMV induce immunopathologic vascular disease exclusively in immunocompromised hosts; e.g. only irradiated mice (52) or rats (53) develop severe arterial inflammation after infection with murine or rat CMV, respectively. In addition, mice lacking the IFN-␥ receptor are more susceptible to infection with murine CMV (54) or gammaherpesvirus 68 (55) and develop progressive chronic arterial inflammation.…”
Section: Discussionmentioning
confidence: 99%
“…In the CMV-infected BALB/c mouse, viral antigens were demonstrable in aortic endothelial and smooth muscle cells, accompanied by inflammatory cells typically seen in atherosclerotic lesions (7), suggesting an inflammatory response induced by the virus. Furthermore viral infection was followed by increased serum concentration of low-density lipoprotein, consistent with yet another mechanism by which the virus might induce atherosclerosis.…”
Section: Animal Modelsmentioning
confidence: 97%
“…Of all evaluated pathogens, only IgG seropositivity to HSV-2 (p = 0.05) and IgA seropositivity to EBV (p = 0.001) as well as H. pylori (p = 0.002) revealed an independent significant association with future cardiovascular death. However, when infectious burden was evaluated, patients seropositive to > 5 pathogens compared with those seropositive to <4 pathogens had a 5.1 (1,(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18) higher risk of future cardiac death. This result was mainly driven by the pathogen burden of seropositivities to Herpes viridae (p < 0.0001).…”
Section: Total Pathogen Burdenmentioning
confidence: 99%
“…TLR3, 7, and 9 may also participate in atherosclerosis (38,39). For example, murine cytomegalovirus exacerbates atherosclerosis and is a ligand for TLR3 and TLR9 (39,40). Coxsackie B virus is an agonist for TLR7 and promotes cardiac lipid accumulation in mice (41).…”
Section: Tlrs and Atherosclerosismentioning
confidence: 99%