Predominant right leg dysfunction without asymmetric muscle inflammation in CD1 Swiss mice with coxsackievirus B1-induced myositis

Abstract

INC) AND L. B. A. VAN DH PUTTL. Predom inant right teg dysfunction w ithout asym m etric m uscle inflammation in C D ! Swiss m ire with Coxsackievirus B l-in d u c e d m yositis. P H Y S IO L B E H A V 5 9 (4 /5 ) 763-76N, 1996.■•-■To establish the existence of predominant right leg involvement in Coxsackievirus B l-induced myositis (CBI myositis) 1S9 neonatal CD! Swiss mice were inoculated with 300 pfu C B I, and regularly observed for posture, mobility, and gait. After 2 and 4 weeks, quantitative comparison of m otor dysfunction o f right and left leg yielded an asymmetry score; on light microscopy mononuclear cell infiltration and m uscle fiber necrosis were quantified in bilateral hamstring muscles, using a five-grade scale (0 -4 ). M otor asym m etries were seen during acute viral myositis as soon as hind leg dysfunction appeared, and animals with a predom inant dysfunction of one leg preserved that preference throughout the observation period. At 2 weeks, mice with predom inant right leg dysfunction i n 1 -34) significantly outnumbered those with predominant left leg dysfunction ( n = 11) ( p = 0.01). At 2 and 4 weeks, infiltration ami necrosis in hamstrings from legs with predominant dysfunction were not higher than in those from contralateral legs, and infiltration in right-sided hamstrings was not higher than in left-sided ones, nor was infiltration at 4 weeks. At 4 weeks right-sided muscles were more necrotic (mean ± SD, L 8 ± 1.5) than left-sided muscles (L I j 1.2; /> ^ 0,03). In the absence of predominant inflammatory disease of the right leg, we interpret the hind leg asymmetry as a preferential use of the left leg, due to left-leggedness, and suggest that in CD1 Swiss mice eft-leggednes is associated with increased susceptibility to CB1 myositis. Coxsackievirus BMyositis Murine Asymmetry Lateralization Pathology

Interactions between multiple genetic determinants in the 5′ UTR and VP1 capsid control pathogenesis of chronic post-viral myopathy caused by coxsackievirus B1

“…The possibility that CVB infection is a factor in the pathogenesis of chronic myopathies is demonstrated by an experimental model where acute cytopathic infection of newborn mice with CVB1 T causes long-term sequelae including inflammation of proximal hind limb skeletal muscle and changes in gait, referred to as weakness (Ray et al, 1979;Strongwater et al, 1984). Expression of clinical weakness is asymmetric, associated with increased muscle necrosis, and does not vary once established (Jongen et al, 1996;Tam et al, 1994). By comparison, myositis peaks around 1 month post-infection (PI) and gradually dissipates by 6 months (Tam et al, 1994).…”