Dang Xin, Koralnik Igor J
Division of Viral Pathogenesis, Beth Israel Deaconess Medical Center, Harvard Medical School, RE 213C, 330 Brookline Avenue, Boston, MA 02215, USA.
Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, RE 213C, 330 Brookline Avenue, Boston, MA 02215, USA.
J Gen Virol. 2006 Sep;87(Pt 9):2533-2537. doi: 10.1099/vir.0.81945-0.
The human polyomavirus JC (JCV) typically infects glial cells and is the aetiological agent of progressive multifocal leukoencephalopathy (PML), which occurs in immunosuppressed individuals. The full-length sequence of a granule cell neuron-tropic JCV variant, JCV(GCN1), associated with lytic infection of granule cell neurons and cerebellar atrophy in a human immunodeficiency virus-infected patient with PML was determined and compared with the sequence of the JCV isolate from the classic PML lesions present in the hemispheric white matter of the same individual (JCV(HWM)). A unique deletion was found in the C terminus of the VP1 gene of JCV(GCN1), which encodes the major capsid protein, resulting in a frame shift and a total change of the C-terminal amino acid sequence of this protein. This deletion was not present in JCV(HWM), suggesting that this mutation may be instrumental in facilitating entry or replication of JCV into granule cell neurons.
人类多瘤病毒JC（JCV）通常感染神经胶质细胞，是进行性多灶性白质脑病（PML）的病原体，该病发生于免疫抑制个体。确定了一种与颗粒细胞神经元嗜性JCV变体JCV（GCN1）的全长序列，该变体与一名患有PML的人类免疫缺陷病毒感染患者的颗粒细胞神经元溶解性感染和小脑萎缩有关，并将其与来自同一个体半球白质中经典PML病变的JCV分离株（JCV（HWM））的序列进行比较。在编码主要衣壳蛋白的JCV（GCN1）的VP1基因C末端发现了一个独特的缺失，导致该蛋白C末端氨基酸序列发生移码和完全改变。JCV（HWM）中不存在这种缺失，表明该突变可能有助于JCV进入颗粒细胞神经元或在其中复制。
