Watanabe I, Preskorn S H
Acta Neuropathol. 1976 Oct 15;36(2):101-15. doi: 10.1007/BF00685273.
A 46-year-old female, with an 11 year history of malignant lymphoreticular disease, developed a neurological illness clinically manifested by a focal mass lesion in the left frontal lobe. In biopsied tissue, immunofluorescence study revealed the presence of JC antigen in the glial cells. Histologically, the lesion was characteristic of PML consisting of PML consisting of focal necrosis in the subcortical white matter, numerous fat laden macrophages and marked hypertrophy of oligodendrocytes and astrocytes. By electron microscopy, hypertrophic astrocytes contained intranuclear viral particles consistent with papova virions and aggregates of intracytoplasmic viral particles consisting of a single to several virions tightly surrounded by a single membrane. The membrane appeared to have been derived from that of the cellular vesicles. Fusion of the virus-associated membrane to the astroglial plasmalemma occurred when the virions appeared to shift towards extracellular space. The virioncontaining astrocytes showed cytoplasmic "fibrillar hypertrophy" similar to the characteristic gigantic astroglias of PML. This fact would provide an additional evidence that these gigantic cells, although lacking identifiable viral structures, were the result of anaplastic transformation by JC virus. Many virus-bearing astroglias were noted to be in the early stage of cellular necrosis, of "edematous degeneration". This further indicates that the JC virus is capable of inducing both lytic and abortive astroglial infections. Many oligodendroglias were hypertrophic due to the presence of intranuclear viral particles and markedly increased numbers of microtubules and free ribosomes in the cytoplasm. Membrane-bound intracytoplasmic viral particles were also noted in the oligodendroglias. Some fat laden macrophages contained large intracytoplasmic viral bodies, presumably originating from phagocytized virus-bearing cells.
一名46岁女性,有11年恶性淋巴网状疾病病史,出现一种神经系统疾病,临床表现为左额叶局灶性肿块病变。在活检组织中,免疫荧光研究显示神经胶质细胞中存在JC抗原。组织学上,病变具有进行性多灶性白质脑病(PML)的特征,包括皮质下白质的局灶性坏死、大量富含脂肪的巨噬细胞以及少突胶质细胞和星形胶质细胞的明显肥大。通过电子显微镜观察,肥大的星形胶质细胞含有与乳头多瘤空泡病毒颗粒一致的核内病毒颗粒以及由单个至几个病毒颗粒紧密被单个膜包围组成的胞质内病毒颗粒聚集体。该膜似乎源自细胞囊泡的膜。当病毒颗粒似乎向细胞外空间移动时,病毒相关膜与星形胶质细胞质膜发生融合。含有病毒颗粒的星形胶质细胞显示出细胞质“纤维性肥大”,类似于PML特征性的巨大星形胶质细胞。这一事实将提供额外证据,表明这些巨大细胞尽管缺乏可识别的病毒结构,但却是由JC病毒间变转化的结果。许多携带病毒的星形胶质细胞被注意到处于细胞坏死的早期阶段,即“水肿变性”阶段。这进一步表明JC病毒能够诱导溶解性和流产性星形胶质细胞感染。许多少突胶质细胞因核内病毒颗粒的存在而肥大,并且细胞质中微管和游离核糖体的数量明显增加。在少突胶质细胞中也观察到膜结合的胞质内病毒颗粒。一些富含脂肪的巨噬细胞含有大的胞质内病毒体,推测源自吞噬携带病毒的细胞。