Abstract

The paper gives an update on the pathogenetic role of viral infection and immune mechanisms in the development of cardiac dilatation at the cellular, ultrastructural, and molecular levels. Particular attention is given to the discussion of the possible role of herpesvirus infection in the mechanisms of cardiomyocyte damage with the direct or indirect impact of viral infection through immunoinflammatory responses. Data on the protective and damaging action of a number of cytokines in the immunopathogenesis of viral myocarditis are considered.

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