[Viral infection and myocardial pathology].
A viral infection is the most frequent cause of myocarditis. A viral invasion and viral-mediated cardiomyocyte lesion stimulate an immune system response directed towards the elimination of viral particles, the destruction of infected myocytes, and the limitation of viral dissemination. Numerous studies have shown that the balance of two subpopulations of CD4+ lymphocytes (T-helpers types 1 and 2) determines the character of the immune response in myocarditis, and that this balance is important at the initial stages of immunization, while the cytotoxic CD8+ lymphocytes participate in the myocardial lesion directly. Disorder in the elimination of activated lymphocytes' clones, the degree of which correlates with the degree of cardiac insufficiency, may be one of the mechanisms of myocarditis progression. Disbalance or defects in the system of the regulatory cytokine network also may lead to the activation of potentially autoreactive T-lymphocytes. A connection between viral myocarditis and dilated cardiomyopathy (DCMP) has been discussed for many years. One of the reasons for DCMP development is a viral invasion into the myocardium. Proteinase A, which induces dystrophin proteolysis, which impedes its function, is an ingredient of enteroviruses. Hence, a viral infection may cause two myocardial diseases: viral (infective-and-immune) myocarditis and DCMP.
Paleev
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D000208:Acute Disease; D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D002311:Cardiomyopathy, Dilated / Q000209:etiology* / Q000276:immunology / Q000821:virology*; D003384:Coxsackievirus Infections / Q000150:complications / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D004195:Disease Models, Animal; D018450:Disease Progression; D006801:Humans; D051379:Mice; D008807:Mice, Inbred BALB C; D009205:Myocarditis / Q000209:etiology* / Q000276:immunology / Q000821:virology*; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D013997:Time Factors; D014777:Virus Diseases / Q000150:complications* / Q000276:immunology
D016207:Cytokines