Lawn A M, Payne L N
Neuropathol Appl Neurobiol. 1979 Nov-Dec;5(6):485-97. doi: 10.1111/j.1365-2990.1979.tb00645.x.
A chronological study was made of the ultrastructural changes in peripheral nerves following inoculation of 1-day-old chicks with a neurogenic strain of Marek Disease virus. No virus particles were found in nerves. Cellular infiltration of nerves was detected as early as 5 days after inoculation and by 3 weeks some nerves contained proliferative lesions which possessed many of the ultrastructural features characteristic of normal, reactive lymphoid tissue. About 4 weeks after inoculation, coinciding with the onset of neurological signs, areas of widespread demyelination appeared within these lesions; lymphocytes and macrophages penetrated and destroyed the myelin sheath, but spared Schwann cells and most axons. Later oedematous, sparsely infiltrated B type lesions were observed, some of which contained demyelinated nerve fibres undergoing repair; these were therefore a stage in the regression of the proliferative lesions. Our observations do not favour the hypothesis that cellular infiltration of nerves in Marek's disease is the direct result of auto-sensitization to normal myelin. They are consistent with the hypothesis that demyelination is a secondary feature and that the primary lesions are preferential sites for immune demyelination.
对1日龄雏鸡接种神经型马立克氏病病毒后外周神经的超微结构变化进行了一项时间顺序研究。在神经中未发现病毒颗粒。接种后5天就检测到神经有细胞浸润,到3周时,一些神经出现增殖性病变,这些病变具有许多正常反应性淋巴组织特有的超微结构特征。接种后约4周,与神经症状的出现同时,这些病变内出现广泛的脱髓鞘区域;淋巴细胞和巨噬细胞穿透并破坏髓鞘,但施万细胞和大多数轴突未受影响。后来观察到水肿、稀疏浸润的B型病变,其中一些含有正在修复的脱髓鞘神经纤维;因此这些是增殖性病变消退的一个阶段。我们的观察结果不支持马立克氏病中神经细胞浸润是对正常髓鞘自身致敏的直接结果这一假说。它们与脱髓鞘是次要特征且原发性病变是免疫性脱髓鞘的优先部位这一假说一致。