Powell H C, Lampert P W
Lab Invest. 1975 Oct;33(4):440-5.
Mice infected with JHM strain of mouse hepatitis virus develop a demyelinating encephalomyelitis. Myelin sheaths are stripped off axons by invading macrophages after degeneration of the infected oligodendrocytes. The derivation of the virus from granular cytoplasmic particles that condense around and bud into endoplasmic reticulum is demonstrated. The infected oligodendrocytes undergo hypertrophic changes prior to degeneration. Hypertrophic cells are characterized by abundant microtubules, filaments, mitochondria, aggregates of electron-dense particles, and numerous, unusual plasma membrane connections to myelin lamellae. Vacular and hydropic changes are prominent in degenerating cells. The significance of finding infected oligodendrocytes with altered myelin-plasma membrane connections is discussed with reference to the pathogenesis of recurrent, postinfectious demyelination known to develop subsequent to acute virus infections.
感染小鼠肝炎病毒JHM株的小鼠会发生脱髓鞘性脑脊髓炎。在被感染的少突胶质细胞变性后,髓鞘被侵入的巨噬细胞从轴突上剥离。已证明该病毒源自聚集在内质网周围并芽生到内质网中的颗粒状细胞质颗粒。被感染的少突胶质细胞在变性前会发生肥大性变化。肥大细胞的特征是有丰富的微管、细丝、线粒体、电子致密颗粒聚集体,以及与髓鞘板有许多异常的质膜连接。血管和水肿变化在变性细胞中很明显。结合急性病毒感染后已知会发生的复发性感染后脱髓鞘的发病机制,讨论了发现具有改变的髓鞘-质膜连接的被感染少突胶质细胞的意义。