Coxsackievirus B cardiopathy and angiopathy in the hypercholesterolemic host.
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 B5. 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.
D000818:Animals; D001011:Aorta / Q000382:microbiology*; D001835:Body Weight; D002318:Cardiovascular Diseases / Q000209:etiology*; D003384:Coxsackievirus Infections / Q000150:complications*; D029822:Enterovirus B, Human / Q000472:pathogenicity; D005455:Fluorescent Antibody Technique; D006937:Hypercholesterolemia / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D008055:Lipids / Q000097:blood; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D014779:Virus Replication
D008055:Lipids