EBV: immunobiology and host response
EBV: immunobiology and host response
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DOI：
10.1017/cbo9780511545313.040
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发表时间：
2007
期刊：
影响因子：
--
通讯作者：
A. Arvin;A. Abendroth
中科院分区：
文献类型：
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作者：
A. Arvin;A. Abendroth
水痘带状疱疹病毒 (VZV) 与其他疱疹病毒家族成员一样，是一种非常成功且普遍存在的人类病原体。为了使水痘带状疱疹病毒在人群中持续存在，该病毒进化出了避免免疫检测并可能促进病毒发病机制的策略。我们已经证明，在原代人包皮成纤维细胞（HFF）的生产性感染过程中，VZV 通过特异性下调细胞表面 MHC Ⅰ 类（Abendroth 等，2001a）和抑制干扰素 γ 诱导的 MHC Ⅱ 类表达上调（Abendroth 等，2000）来编码两种独立的免疫逃避策略。鉴于 VZV 似乎在 10-21 天的漫长潜伏期内逃避了 T 细胞的识别，编码免疫调节蛋白的病毒基因可能会延迟 VZV 特异性 CD4+ 和 CD8+ T 淋巴细胞的初始克隆扩增，并至少暂时增强 VZV 在皮肤部位复制的能力。最近我们研究了 VZV 与人树突状细胞 (DC) 和 T 淋巴细胞的相互作用。 VZV 具有感染未成熟 DC 并将病毒转移至 T 淋巴细胞的能力（Abendroth 等，2001b）。 VZV 也很容易感染扁桃体 T 细胞（Ku 等，2002）。第 37 章描述了病毒发病机制期间 VZV 与 T 细胞相互作用的分析。VZV 感染 DC 和 T 细胞的这些能力提供了原发性和复发性 VZV 感染期间病毒传播的新模型。评估成熟 DC 的进一步研究揭示了 VZV 的第三种免疫逃避机制，即病毒能够有效地感染专门的免疫细胞（代表最有效的抗原呈递细胞类型），并在此过程中损害其正常功能的能力。
Varicella zoster virus (VZV) like the other herpesvirus family members is a highly successful and ubiquitous human pathogen. In order for VZV to persist in the human population, the virus has evolved strategies to avoid immune detection and potentially promote viral pathogenesis. We have demonstrated that VZV encodes two separate immune evasion strategies by specifically down-regulating cell-surface MHC class Ⅰ (Abendroth et al., 2001a) and inhibiting the up-regulation of interferon-γ-induced MHC class Ⅱ expression (Abendroth et al., 2000) during productive infection of primary human foreskin fibroblasts (HFFs). Given that VZV appears to evade host recognition by T-cells during the prolonged, 10–21 day incubation period, viral genes encoding immunomodulatory proteins are likely to delay the initial clonal amplification of VZV specific CD4+ and CD8+ T-lymphocytes and at least transiently enhance the ability of VZV to replicate at cutaneous sites. Recently we have studied the interaction of VZV with human dendritic cells (DCs) and T-lymphocytes. VZV has the ability to infect immature DCs and transfer virus to T-lymphocytes (Abendroth et al., 2001b). VZV also readily infects tonsil T-cells (Ku et al., 2002). The analysis of VZV interactions with T-cells during viral pathogenesis is described in Chapter 37. These capacities of VZV to infect DC and T-cells provide new models of viral dissemination during primary and recurrent VZV infections. Further studies assessing mature DCs have revealed a third immune evasion mechanism for VZV whereby the virus is able to productively infect a specialized immune cell (representing the most potent antigen presenting cell type), and in doing so impairs its ability to function properly.