Neurotropic RNA viruses continue to emerge and are increasingly linked to diseases of the central nervous system (CNS) despite viral clearance. Indeed, the overall mortality of viral encephalitis in immunocompetent individuals is low, suggesting efficient mechanisms of virologic control within the CNS. Both immune and neural cells participate in this process, which requires extensive innate immune signaling between resident and infiltrating cells, including microglia and monocytes, that regulate the effector functions of antiviral T and B cells as they gain access to CNS compartments. While these interactions promote viral clearance via mainly neuroprotective mechanisms, they may also promote neuropathology and, in some cases, induce persistent alterations in CNS physiology and function that manifest as neurologic and psychiatric diseases. This review discusses mechanisms of RNA virus clearance and neurotoxicity during viral encephalitis with a focus on the cytokines essential for immune and neural cell inflammatory responses and interactions. Understanding neuroimmune communications in the setting of viral infections is essential for the development of treatments that augment neuroprotective processes while limiting ongoing immunopathological processes that cause ongoing CNS disease.

中文翻译：

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RNA 病毒感染期间的神经炎症。


尽管病毒被清除，嗜神经性 RNA 病毒仍在不断出现，并且与中枢神经系统 (CNS) 疾病的联系越来越紧密。事实上，免疫功能正常的个体中病毒性脑炎的总体死亡率较低，这表明中枢神经系统内存在有效的病毒学控制机制。免疫细胞和神经细胞都参与这一过程，这需要常驻细胞和浸润细胞（包括小胶质细胞和单核细胞）之间存在广泛的先天免疫信号传导，当抗病毒 T 细胞和 B 细胞进入 CNS 区室时，这些细胞可调节它们的效应功能。虽然这些相互作用主要通过神经保护机制促进病毒清除，但它们也可能促进神经病理学，在某些情况下，诱导中枢神经系统生理和功能的持续改变，表现为神经系统和精神疾病。这篇综述讨论了病毒性脑炎期间 RNA 病毒清除和神经毒性的机制，重点关注免疫和神经细胞炎症反应和相互作用所必需的细胞因子。了解病毒感染情况下的神经免疫通讯对于开发增强神经保护过程的治疗方法至关重要，同时限制导致持续中枢神经系统疾病的持续免疫病理过程。