爱泼斯坦-巴尔病毒（EBV）的潜伏膜蛋白2A（LMP2A）在B细胞受体激活后会改变正常的转录调控。

Epstein-Barr virus (EBV) LMP2A alters normal transcriptional regulation following B-cell receptor activation.

作者信息

Portis Toni, Longnecker Richard

机构信息

Department of Microbiology and Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.

出版信息

Virology. 2004 Jan 20;318(2):524-33. doi: 10.1016/j.virol.2003.09.017.

DOI:10.1016/j.virol.2003.09.017

PMID:14972521

Abstract

The latent membrane protein 2A (LMP2A) of Epstein-Barr virus (EBV) is an important mediator of viral latency in infected B-lymphocytes. LMP2A inhibits B-cell receptor (BCR) signaling in vitro and allows for the survival of BCR-negative B cells in vivo. In this study, we compared gene transcription in BCR-activated B cells from non-transgenic and LMP2A Tg6 transgenic mice. We found that the transcriptional induction and down-regulation of many genes that normally occurs in B cells following BCR activation did not occur in B cells from LMP2A Tg6 transgenic mice. Furthermore, LMP2A induced the expression of various transcription factors and genes associated with DNA/RNA metabolism, which may allow for the altered transcriptional regulation observed in BCR-activated B cells from LMP2A Tg6 mice. These results suggest that LMP2A may inhibit the downstream effects of BCR signaling by directly or indirectly altering gene transcription to ensure EBV persistence in infected B cells.

摘要

爱泼斯坦-巴尔病毒（EBV）的潜伏膜蛋白2A（LMP2A）是受感染B淋巴细胞中病毒潜伏的重要介质。LMP2A在体外抑制B细胞受体（BCR）信号传导，并使BCR阴性B细胞在体内存活。在本研究中，我们比较了来自非转基因和LMP2A Tg6转基因小鼠的BCR激活B细胞中的基因转录。我们发现，BCR激活后正常发生在B细胞中的许多基因的转录诱导和下调在LMP2A Tg6转基因小鼠的B细胞中并未发生。此外，LMP2A诱导了与DNA/RNA代谢相关的各种转录因子和基因的表达，这可能导致在LMP2A Tg6小鼠的BCR激活B细胞中观察到转录调控的改变。这些结果表明，LMP2A可能通过直接或间接改变基因转录来抑制BCR信号传导的下游效应，以确保EBV在受感染B细胞中的持续存在。