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对鼠γ-疱疹病毒的特异性宿主反应的动力学分析。

Kinetic analysis of the specific host response to a murine gammaherpesvirus.

作者信息

Stevenson P G, Doherty P C

机构信息

Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.

出版信息

J Virol. 1998 Feb;72(2):943-9. doi: 10.1128/JVI.72.2.943-949.1998.

DOI:10.1128/JVI.72.2.943-949.1998
PMID:9444986
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC124564/
Abstract

Respiratory infection of BALB/c mice with the murine gammaherpesvirus 68 (MHV-68) induces the clonal expansion of virus-specific cytotoxic T-lymphocyte (CTL) precursors (CTLp) in the regional, mediastinal lymph nodes (MLN). Some of these CTLps differentiate to become fully functional CTL effectors, which can be detected in both the lymphoid tissue and in the site of pathology in the lung. Though the lymph nodes and spleen harbor substantial populations of latently infected B cells for life, the level of virus-specific CTL activity decreases rapidly in all sites. The CD8+ CTLp numbers fall to background levels in the MLN within several months of the termination of the productive phase of MHV-68 infection in the respiratory epithelium but are maintained at relatively low frequency in the spleen. The continued presence of a gamma interferon-producing, MHV-68-specific CD4+ set can also be demonstrated in cultured spleen cells. The virus-specific immunoglobulin G (IgG) response is slow to develop, with serum neutralizing antibody and enzyme-linked immunosorbent assay titers continuing to rise for several months. The level of total serum IgG increases dramatically within 2 weeks of infection, probably as a consequence of polyclonal B-cell activation, and remains high. The immune response profile is clearly influenced by the persistence of this DNA virus.

摘要

用鼠γ疱疹病毒68(MHV - 68)感染BALB/c小鼠的呼吸道,可诱导区域纵隔淋巴结(MLN)中病毒特异性细胞毒性T淋巴细胞(CTL)前体(CTLp)的克隆扩增。其中一些CTLp分化成为功能完全的CTL效应细胞,在淋巴组织和肺脏的病理部位均可检测到。虽然淋巴结和脾脏终生都含有大量潜伏感染的B细胞,但病毒特异性CTL活性在所有部位均迅速下降。在呼吸道上皮中MHV - 68感染的增殖期结束后的几个月内,MLN中的CD8⁺ CTLp数量降至背景水平,但在脾脏中维持在相对较低的频率。在培养的脾细胞中也可证明存在产生γ干扰素的、MHV - 68特异性CD4⁺细胞群。病毒特异性免疫球蛋白G(IgG)反应发展缓慢,血清中和抗体和酶联免疫吸附测定滴度持续上升数月。感染后2周内血清总IgG水平急剧升高,可能是多克隆B细胞活化的结果,并保持在高水平。这种DNA病毒的持续存在显然影响了免疫反应谱。

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本文引用的文献

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Immunological control of murine gammaherpesvirus infection is independent of perforin.小鼠γ疱疹病毒感染的免疫控制不依赖于穿孔素。
J Gen Virol. 1997 Aug;78 ( Pt 8):2025-30. doi: 10.1099/0022-1317-78-8-2025.
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Murine gammaherpesvirus 68 encodes tRNA-like sequences which are expressed during latency.鼠γ疱疹病毒68编码在潜伏期间表达的tRNA样序列。
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Bone marrow can function as a lymphoid organ during a primary immune response under conditions of disrupted lymphocyte trafficking.在淋巴细胞运输受阻的情况下,骨髓在初次免疫反应期间可发挥淋巴器官的功能。
J Immunol. 1997 Apr 15;158(8):3716-20.
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Gamma interferon is not essential for recovery from acute infection with murine gammaherpesvirus 68.γ干扰素对于从鼠γ疱疹病毒68急性感染中恢复并非必不可少。
J Virol. 1997 May;71(5):3916-21. doi: 10.1128/JVI.71.5.3916-3921.1997.
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Progressive loss of CD8+ T cell-mediated control of a gamma-herpesvirus in the absence of CD4+ T cells.在缺乏CD4 + T细胞的情况下,CD8 + T细胞介导的对γ-疱疹病毒的控制作用逐渐丧失。
J Exp Med. 1996 Sep 1;184(3):863-71. doi: 10.1084/jem.184.3.863.
8
A mouse cytomegalovirus glycoprotein, gp34, forms a complex with folded class I MHC molecules in the ER which is not retained but is transported to the cell surface.一种小鼠巨细胞病毒糖蛋白gp34,在内质网中与折叠的I类主要组织相容性复合体分子形成复合物,该复合物不会被滞留,而是被转运到细胞表面。
EMBO J. 1997 Feb 17;16(4):685-94. doi: 10.1093/emboj/16.4.685.
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The HCMV gene products US11 and US2 differ in their ability to attack allelic forms of murine major histocompatibility complex (MHC) class I heavy chains.人巨细胞病毒基因产物US11和US2在攻击小鼠主要组织相容性复合体(MHC)I类重链等位基因形式的能力上存在差异。
J Exp Med. 1997 Jan 20;185(2):363-6. doi: 10.1084/jem.185.2.363.
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Inflammatory infiltration of the upper airway epithelium during Sendai virus infection: involvement of epithelial dendritic cells.仙台病毒感染期间上呼吸道上皮的炎性浸润:上皮树突状细胞的作用
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