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Coxsackievirus B cardiopathy and angiopathy in the hypercholesterolemic host

  • Ann E. Campbell
    Affiliations
    Departments of Microbiology and Academic Pathology, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298 U.S.A.
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  • Roger M. Loria
    Footnotes
    Affiliations
    Departments of Microbiology and Academic Pathology, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298 U.S.A.
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  • Gordon E. Madge
    Affiliations
    Departments of Microbiology and Academic Pathology, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298 U.S.A.
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  • Author Footnotes
    1 Dr. Roger Loria is a recipient of the American Diabetes Association, Inc. Young Investigator Award. Please address reprint requests to Roger M. Loria, Ph.D., Department of Microbiology, Box 847, MCV Station, Richmond, VA 23298, U.S.A.
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      Abstract

      Studies on the pathogenic potential of the human cardiotropic enterovirus, coxsackievirus B5, show that this agent localizes and replicates in the aorta of mice. Nutritionally-induced hypercholesterolemia leads to an increased replication and persistence of virus in tissues, specifically the aorta. Coxsackievirus B cardiopathy is markedly augmented in the hypercholesterolemic host, resulting in a persistent cardiomyolysis which is not evident in virus-infected animals with normal cholesterol levels. Pathological changes in the aorta become evident only months after the acute infection, and only in hypercholesterolemic animals previously infected with coxsackievirus 135.
      Our findings of coxsackievirus B-induced angiopathy and cardiopathy in the hypercholesterolemic host extend the known pathogenic range of these human viruses, and further emphasizes their potential as etiological agents of cardiovascular disease.

      Keywords

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