A non-cardiovirulent strain of coxsackievirus B3 causes myocarditis in mice with severe combined immunodeficiency syndrome.
The most extensively studied animal model of coxsackievirus B3 (CVB3)-induced inflammatory heart muscle disease is the murine model. In the acute and chronic phase of the disease, it has been suggested that autoimmune mechanisms play a major role in the pathogenesis of the disease. In this study, C3H mice without functional T- and B-lymphocytes (C3H SCID) were inoculated either with a cardiovirulent (CVB3/20) or a non-cardiovirulent (CVB3/0) strain of coxsackievirus B3. Both viruses caused myocarditis in SCID mice. Furthermore, it could be demonstrated, that CVB3/0 had mutated to a cardiovirulent phenotype, able to cause myocarditis in immunocompetent mice.
Hufnagel
G
G
Philipps University of Marburg, Department of Cardiology, Germany.
Chapman
N
N
Tracy
S
S
D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology / Q000473:pathology / Q000821:virology; D003384:Coxsackievirus Infections / Q000276:immunology* / Q000473:pathology / Q000821:virology; D004195:Disease Models, Animal; D029822:Enterovirus B, Human / Q000145:classification / Q000235:genetics / Q000472:pathogenicity*; D007108:Immune Tolerance / Q000276:immunology; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D016513:Mice, SCID; D009154:Mutation; D009205:Myocarditis / Q000276:immunology* / Q000473:pathology / Q000821:virology; D009206:Myocardium / Q000276:immunology / Q000473:pathology; D014774:Virulence / Q000235:genetics