Identification of the site of Epstein-Barr virus persistence in vivo as a resting B cell
Identification of the site of Epstein-Barr virus persistence in vivo as a resting B cell
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DOI：
10.1128/jvi.71.7.4882-4891.1997
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发表时间：
1997-07-01
影响因子：
5.4
通讯作者：
ThorleyLawson, DA
中科院分区：
文献类型：
--
作者：
Miyashita, EM;Yang, B;ThorleyLawson, DA
EB病毒(Epstein-Barr，EBV)是一种强大的体外人类B淋巴细胞永生化病毒，与体内几种人类肿瘤相关。以前，我们已经证明，在健康、持续感染的人的外周血中，大多数EBV感染的细胞不表达激活的表型，例如，高水平的细胞表面CD23和CD80(B7)，在体外永生的细胞上表达的特征是，我们在这里表明，大于或等于90%的CD23(-)，病毒感染的细胞在外周血中处于G(0)，因此休息，剩余的细胞可能被G(1)滞留，但我们无法检测到相当数量的细胞穿过S-G(2)-M期的细胞周期。在该人群中很容易检测到来源于Q(P)的LMP2A型而不是EBNA1型的mRNA，而且这些细胞似乎具有处理和呈递抗原的能力，我们认为这些静息的B细胞是EBV长期潜伏持续的部位，我们进一步认为病毒在静息的B7(-)B细胞中的持续是逃避免疫监视的重要机制。EBV-tan在静息B细胞中潜伏存在意味着EBV永生化功能在正常B细胞中可以下调，这一结论对认识和控制EBV相关肿瘤具有重要意义。
Epstein-Barr (EBV) is a powerful immortalizing virus for human B lymphocytes in vitro and is associated with several human neoplasias in vivo, Previously, we have shown that the majority of EBV-infected cells in the peripheral blood of healthy, persistently infected individuals do not express the activated phenotype, e.g., high levels of cell surface CD23 and CD80 (B7), characteristically expressed on in vitro-immortalized cells, Here, we show that greater than or equal to 90% of the CD23(-), virus-infected cells in the peripheral blood are in G(0) and therefore resting, The remaining cells may be G(1) arrested, but we were unable to detect a significant number of cells traversing the S-G(2)-M stages of the cell cycle. The mRNA for LMP2A, but not EBNA1 originating from Q(p), mas readily detected in this population, and these cells appear competent in the processing and presentation of antigen by class 1 major histocompatibility complex, We propose that these resting B cells are the site of long-term latent persistence for EBV, We further propose that the persistence of the virus in a resting B7(-) B cell provides an important mechanism to escape immunosurveillance. The demonstration that EBV tan persist latently in a resting B cell means that the immortalizing functions of EBV can be down regulated in a normal B cell, This conclusion has important implications for understanding and controlling EBV-associated neoplasia.