Infection of adolescent CD-1 mice with CVB3 activates NK cells. These activated NK cells can lyse infected fibroblasts in vitro and their transfer into mice prior to inoculation with CVB3 can reduce virus titers in heart tissues. If mice are depleted of NK cells prior to and throughout a CVB3 infection, myocarditic lesions show a comparatively greater pathology in the form of severe dystrophic calcification than in infected mice with an intact NK cell system. Also NK cell-depleted mice have significantly higher virus titers in heart tissues. These data suggest a role for NK cells in the infected mouse, i. e., that they reduce virus titers through lysis of infected cells and thereby reduce the severity of myocarditis. In keeping with such a defensive role is the finding of NK cells among the first inflammatory cells forming the nascent CVB3-induced focal myocarditic lesion. Paradoxically, NK cells remain in the mature lesion up to 10 days p.i. and may thus contribute to pathology. Further studies on whether these long-term residents release cytotoxic factors which continue to damage myocytes in absence of significant virus titers in heart tissues must be performed. These studies are now feasible because of the recent development of monoclonal antibodies against NK cytotoxic factor . Finally, diet can adversely effect generation of activated NK cells in CVB3-inoculated mice and this finding may have significance for health-conscious human beings.
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