Genetic control of Coxsackievirus B3-induced heart-specific autoantibodies associated with chronic myocarditis

Cardiac-specific autoantibodies to sarcolemmal and cardiac myosin antigens observed during the chronic phase of Coxsackievirus B3-induced myocarditis appear to be under autosomal recessive control. This observation is based on examination of F1 hybrids bred from A/J mice which develop chronic myocarditis and C57BL/6J mice which resolve the virus-induced lesions. Previous mouse studies demonstrated that the prevalence of heart-specific autoantibodies varied with the H-2 complex. However, in 25 H-2 congenic mouse strains the strain background was the predominant determinant of autoantibody presence. Recently, we extended our genetic evaluation of the chromosomal locations governing autoantibody responses by examining 25 AXB and BXA recombinant inbred strains. Two populations of heart-specific autoantibodies were demonstrated against sarcolemmal and cardiac myosin antigens. Analyses of the AXB/BXA strain distribution patterns for these two traits revealed that the anti-sarcolemmal response was controlled by a gene(s) linked to Np-2 and Ter alpha loci on chromosome 14. Linkage could not be assigned for the anti-cardiac myosin response.