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. 2015 Sep 16;10(9):e0138222. doi: 10.1371/journal.pone.0138222

Fig 1. Differential susceptibility to viral myocarditis is controlled by a chr. 7 locus.

Fig 1

Cardiac viral titer and histopathology were examined in 129S1 and 129X1 mice infected with 500pfu/g CVB3. Viral titer was equal between both strains (A). 129S1 mice developed calcified lesions (B, E) and increased inflammation (C, F) in response to CVB3 infection. 129X1 mice very rarely presented with either (D, E, F). Analysis of phenotypic segregation and linkage mapping in an (129S1 x 129X1) F2 population identified a common, highly significant locus for each phenotype (Calcification: LOD = 8.307, P<0.0001; Inflammation: LOD = 6.370, P<0.0001) (G). Peak linkage for both traits occurred on Chr. 7 between markers D7Mit69 (56.3 Mbp) and rs32401703 (68.2 Mbp) (H). Recessive inheritance of homozygous S1 alleles conferred susceptibility to both phenotypes (I,J). Statistical tests were chi-squared test and student’s t test for panels E and F respectively. *** P<0.001. Bar = 50m.