A Murine Model of Polymyositis Induced by Coxsackievirus B1 (Tucson Strain)

Abstract

A murine model of polymyositis induced by coxsackievirus B1, Tucson strain (CVBT) is described. Intraperitoneal CVBT inoculation of CD 1 Swiss mice less than 48 hours old resulted in proximal hindquarter weakness that was first apparent 7 days after viral challenge and persisted for more than 10 weeks. Electromyographic and histologic evidence of a continuing myositis was present during this entire period of time. However, virus was not detectable later than 2 weeks post infection, despite clinical progression of disease. The finding of electromyographir and histologic abnormalities in CVBT-infected mice, long after virus had cleared and neutralizing antibody production evoked, suggests that persistent myositis may be immunologically mediated, triggered by the initial acute viral infection.Polymyositis (PM) is a treatable myopathic disease whose etiology is unknown. Prcvious investigations of this disorder have centered on examining the role of viral infection and autoimmune dysfunction in the pathogenesis of PM, but to date these studies have failed to provide an understanding of the pathogenetic mechanisms involved (1). Further progress in

Anticytoskeletal autoantibodies in the connective tissue diseases

“…In the present study and in patients with acute viral infections, anti-INFIL were nearly always IgM. Second, a coxsackievirusinduced murine polymositis has been recently described (33). In our study, those patients with the highest frequency and the higher titers of anti-INFIL were those with PM/DM.…”

Viral and host genetic factors influence encephalomyocarditis virus—induced polymyositis in adult mice

“…These differences suggest that there are subgroups of idiopathic myositis that have different etiologies. Previous studies have been directed toward developing and studying coxsackievirus-induced myositis as a model for human disease (16,36,37). These models, however, may be more representative of the juvenile type of idiopathic inflammatory myopathies, for the following reasons: (a) neonatal animals and human infants are the most susceptible to coxsackievirus-induced disease, while adults are often resistant (7,11,15,38); and (b) the only controlled investigation showing serologic evidence for the role of coxsackievirus in human myositis is from the study of children with DM (2).…”

“…Coxsackieviruses, which belong to the enterovirus subgroup of Picornuviridue, have been shown to induce myocarditis (1 1-15) and polymyositis (PM) (16) in neonatal mice and have been investigated in attempts to better understand the pathogenesis of inflammatory myopathies. Equivalent models of PM in adult mice with mature immune systems, however, have not been reported.…”

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

“…INOCULATION of the Tucson strain of Coxsackievirus Bl (C'BI) in neonatal CD1 Swiss mice causes, within I week after infection, an acute viral myositis of the hind leii musculature, histologically characterized by widespread necrosis of muscle fibers and diffuse infiltration of polymorphonuclear and m ononu clear cells (22,27,32). Abnormalities in posture and gait appear a few days later (22,27,32).…”