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Query: UMLS:C0027121 (
myositis
)
4,538
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Inoculation of Coxsackie B1 virus (CB1) in newborn
CD1
Swiss mice induces a chronic
myositis
of proximal hindlimb muscles (CB1
myositis
). To study the possible role of the virus dose, and of antiviral antibodies in the development of CB1
myositis
, we infected groups of newborn mice with six CB1 doses, ranging from 30 to 10,000 plaque forming units (pfu); after 4 and 8 weeks we determined morbidity and antiviral antibody titer, and quantified histopathological changes. At 4 weeks, morbidity and mononuclear cell infiltration differed significantly for the various groups, with the most prominent changes in 300 pfu animals. At 4 and 8 weeks diseased animals had significantly higher antibody titers than clinically unaffected animals, and at 4 weeks myopathic and infiltrative changes correlated positively with the serum antibody titer. Our data indicate that the virus dose plays a pathogenic role in CB1
myositis
, and they suggest further study on the role of humoral immune mechanisms in the early phase of CB1
myositis
.
...
PMID:Coxsackie B1 virus-induced murine myositis: relationship of disease severity to virus dose and antiviral antibody response. 817 48
The persistence of coxsackievirus B1 in the muscles of mice with coxsackievirus B1-induced chronic
myositis
was investigated. Neonatal
CD1
Swiss mice were inoculated with a
myositis
-causing variant of coxsackievirus B1 (Tucson strain). Hamstring muscle samples of diseased mice obtained at various times after inoculation were examined for the presence of infectious virus, viral RNA and histological abnormalities. Viral RNA was detected up to 4 weeks after initiation of infection, whereas virus could be isolated from hamstring muscles for up to 2 weeks. Thereafter no sign of infection was demonstrated although histological abnormalities remained present for the entire observation period of 16 weeks. That viral RNA was detectable for only 2 weeks after tissues became negative for infectious virus suggests that the infection slowly waned rather than the viral RNA persisting. Hence, it is concluded that coxsackievirus B1 plays an essential role in the initiation of
myositis
but not in the maintenance of the chronic phase.
...
PMID:Coxsackievirus B1-induced murine myositis: no evidence for viral persistence. 840 31
To establish the existence of predominant right leg involvement in Coxsackievirus B1-induced
myositis
(CB1
myositis
) 189 neonatal
CD1
Swiss mice were inoculated with 300 pfu CB1, and regularly observed for posture, mobility, and gait. After 2 and 4 weeks, quantitative comparison of motor dysfunction of right and left leg yielded an asymmetry score; on light microscopy mononuclear cell infiltration and muscle fiber necrosis were quantified in bilateral hamstring muscles, using a five-grade scale (0-4). Motor asymmetries were seen during acute viral
myositis
as soon as hind leg dysfunction appeared, and animals with a predominant dysfunction of one leg preserved that preference throughout the observation period. At 2 weeks, mice with predominant right leg dysfunction (n = 34) significantly outnumbered those with predominant left leg dysfunction (n = 11) (p = 0.01). At 2 and 4 weeks, infiltration and 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, 1.8 +/- 1.5) than left-sided muscles (1.1 +/- 1.2; p = 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 left-leggedness is associated with increased susceptibility to CB1
myositis
.
...
PMID:Predominant right leg dysfunction without asymmetric muscle inflammation in CD1 Swiss mice with coxsackievirus B1-induced myositis. 877 64