Latent herpesvirus infection in human trigeminal ganglia causes chronic immune response
Latent herpesvirus infection in human trigeminal ganglia causes chronic immune response
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DOI：
10.1016/s0002-9440(10)63575-4
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发表时间：
2003-12-01
影响因子：
6
通讯作者：
Brandt, T
中科院分区：
文献类型：
--
作者：
Theil, D;Derfuss, T;Brandt, T
大多数三叉神经节（TG）潜伏感染α-疱疹病毒[单纯疱疹病毒1型（HSV-1）和水痘-带状疱疹病毒（VZV）]。HSV-1在TG中周期性地重新激活，而VZV很少重新激活。本研究的目的是确定疱疹病毒潜伏期是否与人类TG中的局部免疫细胞浸润有关。在21名健康人的42个检查的TG中，有30个发现了CD 3和CD 8标记物阳性的T细胞和CD 68阳性的巨噬细胞。免疫细胞的存在与HSV-1潜伏相关转录本（LAT）的发生持续相关，仅与潜伏VZV蛋白的存在不规则相关。相比之下，未感染的TG显示没有免疫细胞浸润。定量RT-PCR显示，CD 8，干扰素-γ，肿瘤坏死因子-α，IP-10，和RANTES转录显着诱导与HSV-1潜伏感染的TG，但在未感染的TG。TG中持续的淋巴细胞浸润和升高的CD 8和细胞因子/趋化因子表达首次证明，人类潜伏性疱疹病毒感染伴随免疫豁免部位的慢性炎症过程，但没有任何神经元破坏。慢性免疫应答似乎维持病毒潜伏期并影响病毒再活化。
The majority of trigeminal ganglia (TGs) are latently infected with a-herpesviruses [herpes simplex virus type-1 (HSV-1) and varicella-zoster virus (VZV)]. Whereas HSV-1 periodically reactivates in the TGs, VZV reactivates very rarely. The goal of this study was to determine whether herpesvirus latency is linked to a local immune cell infiltration in human TGs. T cells positive for the CD3 and CD8 markers, and CD68-positive macrophages were found in 30 of 42 examined TGs from 21 healthy individuals. The presence of immune cells correlated constantly with the occurrence of the HSV-1 latency-associated transcript (LAT) and only irregularly with the presence of latent VZV protein. In contrast, uninfected TGs showed no immune cell infiltration. Quantitative RT-PCR revealed that CD8, interferon-gamma, tumor necrosis factor-alpha, IP-10, and RANTES transcripts were significantly induced in TGs latently infected with HSV-1 but not in uninfected TGs. The persisting lymphocytic cell infiltration and the elevated CD8 and cytokine/chemokine expression in the TGs demonstrate for the first time that latent herpesviral infection in humans is accompanied by a chronic inflammatory process at an immunoprivileged site but without any neuronal destruction. The chronic immune response seems to maintain viral latency and influence viral reactivation.