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病毒-受体相互作用对神经致病性和非神经致病性小鼠白血病病毒在大鼠神经胶质细胞中不同病毒增殖的作用。

Contribution of virus-receptor interaction to distinct viral proliferation of neuropathogenic and nonneuropathogenic murine leukemia viruses in rat glial cells.

作者信息

Takase-Yoden S, Watanabe R

机构信息

Institute of Life Science, Soka University, Hachioji, Tokyo 192-8577, Japan.

出版信息

J Virol. 1999 May;73(5):4461-4. doi: 10.1128/JVI.73.5.4461-4464.1999.

DOI:10.1128/JVI.73.5.4461-4464.1999
PMID:10196347
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC104233/
Abstract

The efficiency of receptor-mediated entry of pseudotyped virus carrying the surface protein (SU) of clone A8, a neuropathogenic variant of Friend murine leukemia virus (FrMLV), to rat glial cell line F10 was 1 order of magnitude greater than that of pseudotyped virus carrying SU of nonneuropathogenic FrMLV clone 57. Introduction of the gene coding for ecotropic MLV receptor on F10 cells (F10-ecoR) into SIRC cells, which are naturally resistant to FrMLV infection, also revealed the difference in receptor recognition between the A8 and the 57 viruses. Our results show that the difference in receptor utilization between A8-SU and 57-SU only partially explains the 3-order-of-magnitude difference in proliferation between A8 and 57 viruses in F10 cells.

摘要

携带Friend小鼠白血病病毒(FrMLV)神经致病变体克隆A8表面蛋白(SU)的假型病毒通过受体介导进入大鼠神经胶质细胞系F10的效率比携带非神经致病FrMLV克隆57的SU的假型病毒高1个数量级。将编码嗜亲性MLV受体的基因导入天然对FrMLV感染具有抗性的SIRC细胞中(F10-ecoR),也揭示了A8病毒和57病毒在受体识别上的差异。我们的结果表明,A8-SU和57-SU在受体利用上的差异仅部分解释了A8和57病毒在F10细胞中增殖能力3个数量级的差异。

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