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本文引用的文献

1
Terminal differentiation into plasma cells initiates the replicative cycle of Epstein-Barr virus in vivo.终末分化为浆细胞启动了爱泼斯坦-巴尔病毒在体内的复制周期。
J Virol. 2005 Jan;79(2):1296-307. doi: 10.1128/JVI.79.2.1296-1307.2005.
2
Epstein-Barr virus infection in ex vivo tonsil epithelial cell cultures of asymptomatic carriers.无症状携带者体外扁桃体上皮细胞培养物中的爱泼斯坦-巴尔病毒感染
J Virol. 2004 Nov;78(22):12613-24. doi: 10.1128/JVI.78.22.12613-12624.2004.
3
Use of gHgL for attachment of Epstein-Barr virus to epithelial cells compromises infection.使用gHgL使爱泼斯坦-巴尔病毒附着于上皮细胞会损害感染。
J Virol. 2004 May;78(10):5007-14. doi: 10.1128/jvi.78.10.5007-5014.2004.
4
Epstein-Barr virus infection of polarized tongue and nasopharyngeal epithelial cells.爱泼斯坦-巴尔病毒对极化舌和鼻咽上皮细胞的感染
Nat Med. 2003 Mar;9(3):307-14. doi: 10.1038/nm830. Epub 2003 Feb 18.
5
Alternate replication in B cells and epithelial cells switches tropism of Epstein-Barr virus.在B细胞和上皮细胞中的交替复制改变了爱泼斯坦-巴尔病毒的嗜性。
Nat Med. 2002 Jun;8(6):594-9. doi: 10.1038/nm0602-594.
6
A defective, rearranged Epstein-Barr virus genome in EBER-negative and EBER-positive Hodgkin's disease.EBER阴性和EBER阳性霍奇金淋巴瘤中存在缺陷且重排的爱泼斯坦-巴尔病毒基因组。
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7
Different functional domains in the cytoplasmic tail of glycoprotein B are involved in Epstein-Barr virus-induced membrane fusion.糖蛋白B胞质尾中的不同功能结构域参与爱泼斯坦-巴尔病毒诱导的膜融合。
Virology. 2001 Nov 10;290(1):106-14. doi: 10.1006/viro.2001.1141.
8
Epstein-Barr virus that lacks glycoprotein gN is impaired in assembly and infection.缺乏糖蛋白gN的爱泼斯坦-巴尔病毒在组装和感染方面存在缺陷。
J Virol. 2000 Dec;74(23):11162-72. doi: 10.1128/jvi.74.23.11162-11172.2000.
9
Epstein-Barr virus lacking glycoprotein gp85 cannot infect B cells and epithelial cells.缺乏糖蛋白gp85的爱泼斯坦-巴尔病毒无法感染B细胞和上皮细胞。
Virology. 2000 Oct 10;276(1):52-8. doi: 10.1006/viro.2000.0531.
10
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.

唾液中分泌的爱泼斯坦-巴尔病毒富含B细胞嗜性糖蛋白gp42。

Epstein-Barr virus shed in saliva is high in B-cell-tropic glycoprotein gp42.

作者信息

Jiang R, Scott R S, Hutt-Fletcher L M

机构信息

Department of Microbiology and Immunology, Louisiana State University Health Sciences Center, Shreveport, 71130, USA.

出版信息

J Virol. 2006 Jul;80(14):7281-3. doi: 10.1128/JVI.00497-06.

DOI:10.1128/JVI.00497-06
PMID:16809335
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1489022/
Abstract

Epstein-Barr virus is an orally transmitted human herpesvirus that infects epithelial cells and establishes latency in memory B lymphocytes. Movement of virus between the two cell types is facilitated by changes in amounts of an envelope glycoprotein, gp42, which are effected by interaction of gp42 with HLA class II in a B cell. Here we used the differential ability of virus to bind to CD21-positive B cells and CD21-negative epithelial cells, which is also influenced by levels of gp42, to determine that the majority of virus shed in saliva is derived from an HLA class II-negative cell.

摘要

爱泼斯坦-巴尔病毒是一种经口传播的人类疱疹病毒,它感染上皮细胞并在记忆B淋巴细胞中建立潜伏感染。病毒在这两种细胞类型之间的移动是由包膜糖蛋白gp42数量的变化所促进的,而gp42数量的变化是由gp42与B细胞中的II类人白细胞抗原(HLA)相互作用所导致的。在这里,我们利用病毒与CD21阳性B细胞和CD21阴性上皮细胞结合能力的差异(这种差异也受gp42水平的影响)来确定,唾液中排出的大部分病毒来源于II类HLA阴性细胞。