Georgsson G, Pálsson P A, Panitch H, Nathanson N, Pétursson G
Acta Neuropathol. 1977 Feb 28;37(2):127-35. doi: 10.1007/BF00692058.
The ultrastructure of visna, a slowly progressive menigo-encephalomyelitis of sheep, was studied in animals sacrificed one month after intracerebral inoculation of visna virus. The major pathological changes, representative of those seen during the first year after infection, consist of inflammation and minor focal destructive lesions of grey and white matter. The inflammatory infiltrates, both subependymal and perivascular as well as of the choroid plexus, were composed mainly of lymphocytes and macrophages with varying numbers of plasma cells. The demyelination seen was of the secondary or Wallerian type. There was no evidence of primary demyelination. Visna virions were not seen in any of the CNS material studied. The ultrastructural findings are compatible with the view that lesions in visna may be induced by a cell-mediated immune response. However, changes characteristic of an autoimmune reaction to myelin antigens were not observed.
对绵羊进行脑内接种维斯纳病毒一个月后处死的动物，研究了维斯纳病（一种绵羊缓慢进展性脑膜脑脊髓炎）的超微结构。这些主要病理变化代表感染后第一年所见到的情况，包括灰质和白质的炎症以及轻微的局灶性破坏性病变。室管膜下、血管周围以及脉络丛的炎性浸润主要由淋巴细胞、巨噬细胞以及数量不等的浆细胞组成。所见的脱髓鞘为继发性或华勒氏型。没有原发性脱髓鞘的证据。在所研究的任何中枢神经系统材料中均未见到维斯纳病毒颗粒。超微结构研究结果与以下观点相符，即维斯纳病的病变可能由细胞介导的免疫反应诱发。然而，未观察到对髓鞘抗原自身免疫反应的特征性变化。
