Jacob L. Chason

Coxsackievirus B3 myocarditis in C3H/HeJ mice: Description of an inbred model and the effect of exercise on virulence

The effect of forced exercise on the development of coxsackievirus 133 myocarditis in inbred C3H/HeJ mice was studied. Four groups of mice (30 per group) were formed: infected-exercised (Group I); infected-unexercised (Group II); uninfected-exercised (Group III); and uninfected unexercised (Group IV). Infected mice were inoculated intraperitoneally with 1.0 × 102.1 TCID50 coxsackievirus 133. Exercised animals were swum daily for 60 minutes on days 1–9. Myocardial viral titers were acutely elevated on day 3 of infection and were augmented significantly by exercise on days 6 and 9. Exercise increased the overall mortality from 0–10% to 20–40%; significantly increased heart: body weight ratios on days 6, 9 and 13; and increased the extent of myocardial fiber necrosis. We have reproduced the acceleration of C133 myocarditis by exercise in the inbred C3H model.

A mouse model of transmural myocardial necrosis due to coxsackievirus B4: observations over 12 months.

The course of coxsackievirus B4 necrotizing myocarditis was studied over a 12-month period in 712 ICR Swiss mice inoculated at less than 48 h of age. Affected animals were sacrificed at intervals until 1 year. Microscopically, focal myocardial necrosis, which was often transmural in extent with mixed inflammatory exudate, and subsequent fibrous replacement were induced in 75% of the examined animals. The left ventricle (63 of 69 subjects, 91.3%), interventricular septum (39 of 69 subjects, 56.5%) and right ventricle (26 of 69 subjects, 37.7%) were most frequently involved. Thinning of the ventricular wall and grossly apparent localized ventricular bulges (aneurysms) were seen in 22 subjects (the left ventricle 16 times, the right ventricle 5 times, and the interventricular septum 5 times). Coronary arteries were normal in all instances.