W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Rm E5132, Baltimore, MD 21205, USA.
Immunol Res. 2010 Jul;47(1-3):123-33. doi: 10.1007/s12026-009-8143-4.
Viral encephalomyelitis is caused by virus infections of neurons in the brain and spinal cord. Recovery is dependent on immune-mediated control and clearance of virus from these terminally differentiated essential cells. Preservation of neuronal function is essential for prevention of neurologic sequelae such as paralysis, seizures and cognitive deficits. Using the model system of Sindbis virus-induced encephalomyelitis in mice, we have shown that immune-mediated clearance of infectious virus from neurons is a noncytolytic process. The major effectors are antibody to the E2 surface glycoprotein produced by B cells, and interferon-gamma produced by T cells. These effectors work in synergy, but neuronal populations differ in their responses to each. Virus is least likely to be cleared from brain neurons and most likely to be cleared from motor neurons in the cervical and thoracic regions of the spinal cord. Because the infected neurons are not eliminated, viral RNA persists and long-term control is needed to prevent virus reactivation. Virus-specific antibody-secreting cells residing in the nervous system after recovery from infection are likely to be important for long-term control.
病毒性脑脊髓炎是由病毒感染大脑和脊髓的神经元引起的。恢复取决于免疫介导的控制和清除这些终末分化的必需细胞中的病毒。保护神经元功能对于预防瘫痪、癫痫发作和认知缺陷等神经后遗症至关重要。我们使用辛德毕斯病毒诱导的小鼠脑脊髓炎模型系统表明，免疫介导的从神经元中清除感染性病毒是非细胞溶解过程。主要效应物是 B 细胞产生的针对 E2 表面糖蛋白的抗体和 T 细胞产生的干扰素-γ。这些效应物协同作用，但神经元群体对每种效应物的反应不同。病毒最不可能从大脑神经元中清除，最有可能从颈椎和胸椎区域的脊髓运动神经元中清除。由于感染的神经元没有被清除，病毒 RNA 持续存在，需要长期控制以防止病毒重新激活。感染后驻留在神经系统中的病毒特异性抗体分泌细胞可能对长期控制很重要。
