Neurotropic strains of mouse hepatitis virus (MHV), a coronavirus, cause acute and chronic demyelinating encephalomyelitis with similarities to the human disease multiple sclerosis. Here, using a lineage-tracking system, we show that some cells, primarily oligodendrocytes (OLs) and oligodendrocyte precursor cells (OPCs), survive the acute MHV infection, are associated with regions of demyelination, and persist in the central nervous system (CNS) for at least 150 d. These surviving OLs express major histocompatibility complex (MHC) class I and other genes associated with an inflammatory response. Notably, the extent of inflammatory cell infiltration was variable, dependent on anatomic location within the CNS, and without obvious correlation with numbers of surviving cells. We detected more demyelination in regions with larger numbers of T cells and microglia/macrophages compared to those with fewer infiltrating cells. Conversely, in regions with less inflammation, these previously infected OLs more rapidly extended processes, consistent with normal myelinating function. Together, these results show that OLs are inducers as well as targets of the host immune response and demonstrate how a CNS infection, even after resolution, can induce prolonged inflammatory changes with CNS region-dependent impairment in remyelination.

小鼠冠状病毒肝炎病毒（MHV）的神经质毒株引起急性和慢性脱髓鞘性脑脊髓炎，与人类疾病多发性硬化症相似。在这里，我们使用谱系跟踪系统显示了一些细胞，主要是少突胶质细胞（OL）和少突胶质细胞前体细胞（OPC），在急性MHV感染中幸存下来，与脱髓鞘区域相关，并持续存在于中枢神经系统（CNS）中）至少150 d。这些幸存的OLs表达主要的组织相容性复合体（MHC）I类和其他与炎症反应相关的基因。值得注意的是，炎性细胞浸润的程度是可变的，取决于CNS中的解剖位置，并且与存活细胞的数量没有明显的相关性。与浸润细胞较少的人相比，我们在T细胞和小胶质细胞/巨噬细胞数量较多的区域检测到更多的脱髓鞘。相反，在炎症较少的区域，这些先前感染的OLs可以更快地扩展过程，这与正常的髓鞘功能一致。总之，这些结果表明OLs也是宿主免疫反应的诱导剂和靶标，并证明了即使在消退后，CNS感染如何也可引起长时间的炎症改变，并引起髓鞘再生的CNS区域依赖性损伤。