Rodriguez M, Siegel L M, Hovanec-Burns D, Bologa L, Graves M C
Department of Neurology, Mayo Clinic, Rochester, Minnesota 55905.
Virology. 1988 Oct;166(2):463-74. doi: 10.1016/0042-6822(88)90517-x.
Infection of the central nervous system by Theiler's murine encephalomyelitis virus (TMEV), a picornavirus, produces chronic demyelinating disease in susceptible mice. In this immunoelectron microscopic study of TMEV infection of neonatal mouse brain cells in culture, TMEV antigen was found on the surfaces of infected oligodendrocytes and astrocytes by labeling with hyperimmune serum from TMEV-infected mice or with rabbit antiserum to purified inactivated DA strain TMEV. Brain-derived macrophages had no TMEV-specific antigen on their surfaces and were not able to maintain productive TMEV infection, even though TMEV antigen was present in the cytoplasm. The presence of TMEV antigens on the surfaces of oligodendrocytes (myelin-producing cells) was unexpected because picornaviruses are nonenveloped viruses and do not bud from cell surfaces. The finding is consistent with the hypothesis that demyelination follows damage of infected oligodendrocytes by immune cells or immunoglobulins that recognize surface virus antigen.
微小核糖核酸病毒——泰勒氏鼠脑脊髓炎病毒(TMEV)感染中枢神经系统会在易感小鼠中引发慢性脱髓鞘疾病。在这项针对培养的新生小鼠脑细胞进行的TMEV感染的免疫电子显微镜研究中,通过用来自TMEV感染小鼠的超免疫血清或用针对纯化的灭活DA株TMEV的兔抗血清进行标记,在受感染的少突胶质细胞和星形胶质细胞表面发现了TMEV抗原。脑源性巨噬细胞表面没有TMEV特异性抗原,即使TMEV抗原存在于细胞质中,它们也无法维持TMEV的有效感染。少突胶质细胞(产生髓磷脂的细胞)表面存在TMEV抗原是出乎意料的,因为微小核糖核酸病毒是无包膜病毒,不会从细胞表面出芽。这一发现与以下假设一致,即脱髓鞘是由识别表面病毒抗原的免疫细胞或免疫球蛋白对受感染的少突胶质细胞造成损伤后发生的。