Immunohistochemical localization of neurotropic ecotropic murine leukemia virus in moribund mice.
Immunohistochemical localization of neurotropic ecotropic murine leukemia virus in moribund mice.
复制标题
垂死小鼠中神经亲嗜性鼠白血病病毒的免疫组织化学定位。
DOI：
10.1016/0042-6822(90)90383-3
复制
发表时间：
1990
期刊：
影响因子：
3.7
通讯作者：
Wiley,CA
中科院分区：
文献类型：
--
作者：
Morey,MK;Wiley,CA
嗜神经性亲嗜性小鼠白血病病毒（NE-MuLV）的CasBrE株感染易感小鼠并诱导非炎症性、缓慢变性的神经系统疾病。我们采用免疫组织化学方法来识别慢性感染小鼠神经系统和其他组织中哪些细胞含有病毒抗原。使用全病毒和对应于病毒包膜蛋白的14个氨基酸序列的合成肽的不同组合制备兔抗病毒血清。颅内接种NE-MuLV的44只新生小鼠中有24只（55%）在3-9个月内出现了从颤抖到后肢瘫痪的症状。随后将其处死，并将其组织用于组织学和免疫组织化学。病毒抗原在中枢神经系统（CNS）外的主要部位是骨骼肌和脾脏。骨骼肌是唯一表现出退行性变化的非神经系统组织，如携带病毒抗原的氧化肌纤维萎缩。在中枢神经系统中，在神经元、内皮细胞和神经胶质细胞中检测到病毒抗原。病毒抗原和星形胶质细胞标志物胶质酸性胶质细胞蛋白（GFAP）的免疫组织化学双标记研究表明，含有病毒抗原的胶质细胞是少突胶质细胞，而不是星形胶质细胞。脑组织损伤包括空泡改变和主要在脑干的神经胶质增生。病毒抗原最丰富的本地化在这些地区的病理变化。在脊髓中观察到不同的模式。尽管在整个脊髓中观察到组织损伤，但病毒抗原位于灰色和白色物质的边界。这些发现表明了直接和间接的病毒介导的中枢神经系统损伤机制。
The CasBrE strain of neurotropic ecotropic murine leukemia virus (NE-MuLV) infects susceptible mice and induces a noninflammatory, slowly degenerative nervous system disease. We employed immunohistochemistry to identify which cells in the nervous system and other tissues contained viral antigen in the chronically infected mouse. Rabbit antiserum to the virus was prepared using different combinations of whole virus and synthetic peptides corresponding to a 14-amino-acid sequence of the viral envelope protein. Twenty-four of forty-four (55%) mice neonates inoculated intracranially with NE-MuLV developed symptoms ranging from tremulousness to hindlimb paralysis within 3–9 months. They were subsequently sacrificed and their tissues used for histology and immunohistochemistry. The major locations of viral antigen outside of the central nervous system (CNS) were skeletal muscle and spleen. Skeletal muscle was the only non-nervous system tissue that exhibited degenerative changes as atrophy of viral antigen-bearing oxidative myofibers. In the CNS, viral antigen was detected in neurons, endothelium, and glial cells. Immunohistochemical double-labeling studies for viral antigen and the astrocytic marker glial acidic fibrillary protein (GFAP) demonstrated that the viral antigen-containing glia were oligodendrocytes and not astrocytes. Tissue damage in the brain consisted of vacuolar changes and gliosis principally in the brainstem. Viral antigen was most abundantly localized in these regions of pathologic change. In the spinal cord a different pattern was observed. Although tissue damage was observed throughout the cord, viral antigen was located at the border of the gray and white matter. These findings indicate direct and indirect virus-mediated mechanisms of damage to the CNS.