JC病毒通过网格蛋白依赖的受体介导的内吞作用进入人类神经胶质细胞。
JC virus enters human glial cells by clathrin-dependent receptor-mediated endocytosis.
作者信息
Pho M T, Ashok A, Atwood W J
机构信息
Department of Molecular Microbiology and Immunology, Brown University, Providence, Rhode Island 02912, USA.
出版信息
J Virol. 2000 Mar;74(5):2288-92. doi: 10.1128/jvi.74.5.2288-2292.2000.
Abstract
The human polyomavirus JC virus (JCV) is the etiologic agent of a fatal central nervous system (CNS) demyelinating disease known as progressive multifocal leukoencephalopathy (PML). PML occurs predominantly in immunosuppressed patients and has increased dramatically as a result of the AIDS pandemic. The major target cell of JCV infection and lytic replication in the CNS is the oligodendrocyte. The mechanisms by which JCV initiates and establishes infection of these glial cells are not understood. The initial interaction between JCV and glial cells involves virus binding to N-linked glycoproteins containing terminal alpha(2-6)-linked sialic acids. The subsequent steps of entry and targeting of the viral genome to the nucleus have not been described. In this report, we compare the kinetics and mechanisms of infectious entry of JCV into human glial cells with that of the related polyomavirus, simian virus 40 (SV40). We demonstrate that JCV, unlike SV40, enters glial cells by receptor-mediated clathrin-dependent endocytosis.
摘要
人类多瘤病毒JC病毒（JCV）是一种致命的中枢神经系统（CNS）脱髓鞘疾病——进行性多灶性白质脑病（PML）的病原体。PML主要发生在免疫抑制患者中，并且由于艾滋病大流行而显著增加。JCV在中枢神经系统中感染和裂解复制的主要靶细胞是少突胶质细胞。JCV启动并建立对这些神经胶质细胞感染的机制尚不清楚。JCV与神经胶质细胞之间的初始相互作用涉及病毒与含有末端α（2-6）连接唾液酸的N-连接糖蛋白结合。病毒基因组进入细胞核的后续步骤尚未描述。在本报告中，我们比较了JCV与相关多瘤病毒猿猴病毒40（SV40）感染人类神经胶质细胞的动力学和机制。我们证明，与SV40不同，JCV通过受体介导的网格蛋白依赖性内吞作用进入神经胶质细胞。
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JC virus enters human glial cells by clathrin-dependent receptor-mediated endocytosis.JC病毒通过网格蛋白依赖的受体介导的内吞作用进入人类神经胶质细胞。
J Virol. 2000 Mar;74(5):2288-92. doi: 10.1128/jvi.74.5.2288-2292.2000.
2
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JC virus binds to primary human glial cells, tonsillar stromal cells, and B-lymphocytes, but not to T lymphocytes.JC病毒可与原代人神经胶质细胞、扁桃体基质细胞和B淋巴细胞结合，但不与T淋巴细胞结合。
J Neurovirol. 2000 Apr;6(2):127-36. doi: 10.3109/13550280009013156.
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Infection of glial cells by the human polyomavirus JC is mediated by an N-linked glycoprotein containing terminal alpha(2-6)-linked sialic acids.人多瘤病毒 JC 对神经胶质细胞的感染是由一种含有末端α(2-6)连接唾液酸的 N 连接糖蛋白介导的。
J Virol. 1998 Jun;72(6):4643-9. doi: 10.1128/JVI.72.6.4643-4649.1998.
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The human polyomavirus, JCV, does not share receptor specificity with SV40 on human glial cells.人类多瘤病毒JCV在人类神经胶质细胞上与SV40不具有相同的受体特异性。
J Neurovirol. 1998 Feb;4(1):49-58. doi: 10.3109/13550289809113481.
7
Evaluation of the role of cytokine activation in the multiplication of JC virus (JCV) in human fetal glial cells.细胞因子激活在人胎儿神经胶质细胞中JC病毒（JCV）增殖中的作用评估。
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JC virus infection of hematopoietic progenitor cells, primary B lymphocytes, and tonsillar stromal cells: implications for viral latency.造血祖细胞、原代B淋巴细胞和扁桃体基质细胞的JC病毒感染：对病毒潜伏的影响。
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