Role of CD4+ (helper) T cells in the pathogenesis of murine cytomegalovirus myocarditis.
Murine cytomegalovirus causes diffuse myocardial lesions in immunologically intact young adult male BALB/cBy mice. The cardiac changes develop in and around the small penetrating blood vessels of the heart where perivascular and interstitial infiltrates of macrophages and lymphocytes accumulate. Focal lesions of the coronary vessels and the endocardium also appear. When infected mice are depleted of CD4+ T lymphocytes, myocardial lesions fail to develop even though virus replication in the heart is enhanced. Contrary wise, when CD4+ cells are adoptively transferred into infected, thymectomized, irradiated, bone marrow-repleted mice, focal perivascular necrotizing lesions of the heart develop. Depletion of CD8+ T lymphocytes fails to influence virus replication and the development of cardiac lesions. Endothelial and endocardial cells appear to be major sites of virus replication in the heart. Delayed hypersensitivity is hypothesized to be the mechanism of cardiac injury in this model system.
Department of Pathology, University of Vermont College of Medicine, Burlington.
J E
JE
Craighead
W B
WB
Martin
S A
SA
Huber
D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000502:physiology*; D003587:Cytomegalovirus / Q000472:pathogenicity / Q000502:physiology; D003586:Cytomegalovirus Infections / Q000276:immunology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009205:Myocarditis / Q000276:immunology* / Q000382:microbiology*; D006377:T-Lymphocytes, Helper-Inducer / Q000502:physiology*; D014779:Virus Replication