Department of Neurology, Center for Neurologic Diseases, Brigham and Women's Hospital, Boston, MA 02115, USA.
Brain. 2009 Dec;132(Pt 12):3318-28. doi: 10.1093/brain/awp200.
Multiple sclerosis is an inflammatory demyelinating disease of the central nervous system (CNS) that is thought to be caused by a combination of genetic and environmental factors. To date, considerable evidence has associated Epstein-Barr virus (EBV) infection with disease development. However, it remains controversial whether EBV infects multiple sclerosis brain and contributes directly to CNS immunopathology. To assess whether EBV infection is a characteristic feature of multiple sclerosis brain, a large cohort of multiple sclerosis specimens containing white matter lesions (nine adult and three paediatric cases) with a heterogeneous B cell infiltrate and a second cohort of multiple sclerosis specimens (12 cases) that included B cell infiltration within the meninges and parenchymal B cell aggregates, were examined for EBV infection using multiple methodologies including in situ hybridization, immunohistochemistry and two independent real-time polymerase chain reaction (PCR) methodologies that detect genomic EBV or the abundant EBV encoded RNA (EBER) 1, respectively. We report that EBV could not be detected in any of the multiple sclerosis specimens containing white matter lesions by any of the methods employed, yet EBV was readily detectable in multiple Epstein-Barr virus-positive control tissues including several CNS lymphomas. Furthermore, EBV was not detected in our second cohort of multiple sclerosis specimens by in situ hybridization. However, our real-time PCR methodologies, which were capable of detecting very few EBV infected cells, detected EBV at low levels in only 2 of the 12 multiple sclerosis meningeal specimens examined. Our finding that CNS EBV infection was rare in multiple sclerosis brain indicates that EBV infection is unlikely to contribute directly to multiple sclerosis brain pathology in the vast majority of cases.
多发性硬化症是一种中枢神经系统(CNS)的炎症性脱髓鞘疾病,被认为是由遗传和环境因素共同作用引起的。迄今为止,大量证据表明 EBV 感染与疾病的发展有关。然而,EBV 是否感染多发性硬化症大脑并直接导致 CNS 免疫病理学仍然存在争议。为了评估 EBV 感染是否是多发性硬化症大脑的特征性特征,使用多种方法检查了包含白质病变的大量多发性硬化症标本(9 例成人和 3 例儿科病例),这些标本具有异质性 B 细胞浸润,以及包含脑膜和实质 B 细胞聚集的第二个多发性硬化症标本队列(12 例),以评估 EBV 感染。这些方法包括原位杂交、免疫组织化学和两种独立的实时聚合酶链反应(PCR)方法,分别检测基因组 EBV 或丰富的 EBV 编码 RNA(EBER)1。我们报告说,通过使用的任何方法,都无法在任何包含白质病变的多发性硬化症标本中检测到 EBV,但在包括几种中枢神经系统淋巴瘤在内的多个 EBV 阳性对照组织中,很容易检测到 EBV。此外,通过原位杂交,我们的第二个多发性硬化症标本队列中未检测到 EBV。然而,我们的实时 PCR 方法能够检测到非常少的 EBV 感染细胞,仅在 12 个研究的多发性硬化症脑膜标本中的 2 个中检测到 EBV 水平低。我们发现 CNS EBV 感染在多发性硬化症大脑中很少见,这表明在大多数情况下,EBV 感染不太可能直接导致多发性硬化症大脑病理学。