Ytterberg S R
J Rheumatol. 1987 Feb;14(1):12-8.
Although the etiology of human polymyositis (PM) remains obscure, group B coxsackieviruses (CVB) have been implicated in disease pathogenesis and a particular strain of type 1 CVB (CVB 1) has been shown to cause in mice an inflammatory myositis which is similar to human PM. After infection of neonatal Swiss mice with active CVB 1, virus replicated to high titers in muscle and produced acute myonecrosis. Viral titers peaked in muscle at Day 7 and virus was undetectable after Day 14. Myocytes regenerated, but a chronic inflammatory myositis, involving principally proximal muscle groups of the hind limbs, was observed by Day 14 and persisted through at least Day 70. Injection of inactivated virus resulted in no clinical or histological disease. Anti-CVB 1 antibody was demonstrated in mice injected with inactivated or active virus pools. This report establishes the need for active virus in the pathogenesis of CVB 1 induced murine PM.
尽管人类多发性肌炎(PM)的病因仍不明确,但B组柯萨奇病毒(CVB)被认为与疾病发病机制有关,并且已证明1型CVB的一种特定毒株(CVB 1)可在小鼠中引起类似于人类PM的炎性肌炎。用活性CVB 1感染新生瑞士小鼠后,病毒在肌肉中大量复制并导致急性肌坏死。病毒滴度在第7天达到峰值,第14天后无法检测到病毒。肌细胞再生,但在第14天观察到慢性炎性肌炎,主要累及后肢近端肌群,并至少持续到第70天。注射灭活病毒未导致临床或组织学疾病。在注射灭活或活性病毒库的小鼠中检测到抗CVB 1抗体。本报告确定了活性病毒在CVB 1诱导的小鼠PM发病机制中的必要性。