Herpesvirus interference with major histocompatibility complex class II-restricted T-cell activation.
作者信息
Wiertz Emmanuel J, Devlin Robert, Collins Helen L, Ressing Maaike E
机构信息
Department of Medical Microbiology, Leiden University Medical Center, P.O. Box 9600, 2300 RC Leiden, The Netherlands.
出版信息
J Virol. 2007 May;81(9):4389-96. doi: 10.1128/JVI.01525-06. Epub 2006 Nov 1.
Abstract
摘要
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Host shutoff during productive Epstein-Barr virus infection is mediated by BGLF5 and may contribute to immune evasion.在爱泼斯坦-巴尔病毒有效感染期间宿主关闭由BGLF5介导，可能有助于免疫逃逸。
Proc Natl Acad Sci U S A. 2007 Feb 27;104(9):3366-71. doi: 10.1073/pnas.0611128104. Epub 2007 Feb 21.
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Messenger RNA turnover and its regulation in herpesviral infection.信使核糖核酸周转及其在疱疹病毒感染中的调控
Adv Virus Res. 2006;66:337-94. doi: 10.1016/S0065-3527(06)66007-7.
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Virus-specific CD4+ T cells: ready for direct attack.
J Exp Med. 2006 Apr 17;203(4):805-8. doi: 10.1084/jem.20060215. Epub 2006 Mar 20.
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Control of Epstein-Barr virus infection in vitro by T helper cells specific for virion glycoproteins.通过针对病毒体糖蛋白的辅助性T细胞在体外控制爱泼斯坦-巴尔病毒感染
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The U(L)41 protein of herpes simplex virus 1 degrades RNA by endonucleolytic cleavage in absence of other cellular or viral proteins.单纯疱疹病毒1型的U(L)41蛋白在没有其他细胞或病毒蛋白的情况下，通过核酸内切酶切割来降解RNA。
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J Exp Med. 2005 Oct 17;202(8):1109-19. doi: 10.1084/jem.20050162. Epub 2005 Oct 10.
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CD4+ T-cell responses to Epstein-Barr virus (EBV) latent-cycle antigens and the recognition of EBV-transformed lymphoblastoid cell lines.CD4 + T细胞对爱泼斯坦-巴尔病毒（EBV）潜伏周期抗原的反应以及对EBV转化的淋巴母细胞系的识别。
J Virol. 2005 Apr;79(8):4896-907. doi: 10.1128/JVI.79.8.4896-4907.2005.
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Viral immune evasion molecules attack the ER peptide-loading complex and exploit ER-associated degradation pathways.病毒免疫逃逸分子攻击内质网肽负载复合体并利用内质网相关降解途径。
Curr Opin Immunol. 2005 Feb;17(1):71-8. doi: 10.1016/j.coi.2004.11.009.
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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.
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