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在小鼠B细胞系中建立潜伏性EB病毒感染及稳定的游离型维持状态。

Establishment of latent Epstein-Barr virus infection and stable episomal maintenance in murine B-cell lines.

作者信息

Haan K M, Aiyar A, Longnecker R

机构信息

Department of Microbiology-Immunology, Northwestern University Medical School, Chicago, Illinois 60611, USA.

出版信息

J Virol. 2001 Mar;75(6):3016-20. doi: 10.1128/JVI.75.6.3016-3020.2001.

DOI:10.1128/JVI.75.6.3016-3020.2001
PMID:11222728
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC115929/
Abstract

Epstein-Barr virus (EBV) is a strict human pathogen for which no small animal models exist. Plasmids that contain the EBV plasmid origin of replication, oriP, and express EBV nuclear antigen 1 (EBNA1) are stably maintained extrachromosomally in human cells, whereas these plasmids replicate poorly in rodent cells. However, the ability of oriP and EBNA1 to maintain the entire EBV episome in proliferating rodent cells has not been determined. Expression of the two human B-cell receptors for EBV on the surfaces of murine B cells allows efficient viral entry that leads to the establishment of latent EBV infection and long-term persistence of the viral genome. Latent gene expression in these cells resembles the latency II profile in that EBNA1 and LMP1 can be detected whereas EBNA2 and the EBNA3s are not expressed.

摘要

爱泼斯坦-巴尔病毒(EBV)是一种严格的人类病原体,不存在小动物模型。含有EBV质粒复制起点oriP并表达EBV核抗原1(EBNA1)的质粒在人类细胞中能稳定地在染色体外维持,而这些质粒在啮齿动物细胞中复制较差。然而,oriP和EBNA1在增殖的啮齿动物细胞中维持整个EBV附加体的能力尚未确定。在鼠B细胞表面表达两种人类EBV B细胞受体可实现高效的病毒进入,从而导致潜伏性EBV感染的建立和病毒基因组的长期持续存在。这些细胞中的潜伏基因表达类似于潜伏期II型,即可以检测到EBNA1和LMP1,而EBNA2和EBNA3s不表达。

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本文引用的文献

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Infectious Epstein-Barr virus lacking major glycoprotein BLLF1 (gp350/220) demonstrates the existence of additional viral ligands.缺乏主要糖蛋白BLLF1(gp350/220)的传染性爱泼斯坦-巴尔病毒证明了其他病毒配体的存在。
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Initiation of DNA replication within oriP is dispensable for stable replication of the latent Epstein-Barr virus chromosome after infection of established cell lines.在感染已建立的细胞系后,oriP内DNA复制的起始对于潜伏性爱泼斯坦-巴尔病毒染色体的稳定复制并非必需。
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Coreceptor restriction within the HLA-DQ locus for Epstein-Barr virus infection.爱泼斯坦-巴尔病毒感染在HLA-DQ基因座内的共受体限制
Proc Natl Acad Sci U S A. 2000 Aug 1;97(16):9252-7. doi: 10.1073/pnas.160171697.
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Epstein-Barr virus lacking latent membrane protein 2 immortalizes B cells with efficiency indistinguishable from that of wild-type virus.缺乏潜伏膜蛋白2的爱泼斯坦-巴尔病毒使B细胞永生化,其效率与野生型病毒无法区分。
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Epstein-Barr virus LMP2A drives B cell development and survival in the absence of normal B cell receptor signals.爱泼斯坦-巴尔病毒LMP2A在缺乏正常B细胞受体信号的情况下驱动B细胞发育和存活。
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