COXSACKIE-VIRUS B-3 MYOCARDITIS IN BALB/C MICE - EVIDENCE FOR AUTOIMMUNITY TO MYOCYTE ANTIGENS

  • 1 January 1984
    • journal article
    • research article
    • Vol. 116  (1) , 21-29
Abstract
Male Balb/c mice inoculated with a heart-adapted variant of coxsackievirus, group B, type 3 (CVB3M), develop extensive myocarditis and cytolytic activity to primary cultures of uninfected and infected myocytes. To elucidate the mechanisms of myocyte injury in myocarditis, 2 distinct cytolytic T-lymphocyte (CTL) populations were isolated by immunoadsorption of lymph node cells to glutaraldehyde-fixed uninfected and infected myocyte monolayers. One population preferentially adsorbed to and lysed uninfected myocytes (autoreactive CTL), while the other adsorbed to and lysed CVB3M-infected myocytes (virus-specific CTL). Neither CTL population adsorbed to monolayers of human cervical carcinoma HeLa, mouse L929, or umbilical cord endothelial cells, or to myocytes infected with a related but nonmyocarditic coxsackievirus B-3 variant (CVB30). While both autoreactive and virus-specific CTL induced myocarditis in vivo, the lesions caused by autoreactive CTL were more extensive and necrotizing than those of virus-specific cells. Evidently, CVB3-induced myocarditis results, in part, from autoimmunity to myocyte antigens.