Abstract：
Epstein-Barr virus (EBV) is deemed a necessary, yet insufficient factor in the development of multiple sclerosis (MS). In this study, myelin basic protein-specific transgenic T cell receptor mice were infected with murid gammaherpesvirus 68 virus (MHV68), an EBV-like virus that infects mice, resulting in the onset neurological deficits at a significantly higher frequency than influenza or mock-infected mice. MHV68 infected mice exhibited signs including optic neuritis and ataxia which are frequently observed in MS patients but not in experimental autoimmune encephalomyelitis mice. MHV68-infected mice exhibited increased focal immune cell infiltration in the central nervous system. Single cell RNA sequencing identified the emergence of a population of B cells that express genes associated with antigen presentation and costimulation, indicating that gammaherpesvirus infection drives a distinct, pro-inflammatory transcriptional program in B cells that may promote autoreactive T cell responses in MS.
摘要：
爱泼斯坦-巴尔病毒(EBV)被认为是必要的，但在多发性硬化症（MS）的发展因素不足。在这项研究中,髓鞘碱性蛋白特异性转基因T细胞受体小鼠感染鼠γ疱疹病毒68病毒（MHV68），一种感染小鼠的EBV样病毒，导致神经缺陷的发作频率明显高于流感或模拟感染的小鼠。MHV68感染的小鼠表现出包括视神经炎和共济失调的体征，这在MS患者中经常观察到，但在实验性自身免疫性脑脊髓炎小鼠中没有观察到。MHV68感染的小鼠在中枢神经系统中表现出增加的局灶性免疫细胞浸润。单细胞RNA测序鉴定了表达与抗原呈递和共刺激相关的基因的B细胞群的出现。表明γ疱疹病毒感染驱动一种独特的，B细胞中的促炎转录程序可能促进MS中的自身反应性T细胞应答。
