Takahashi K, Goto N, Matsubara Y, Fujiwara K
Department of Veterinary Pathology, Faculty of Agriculture, University of Tokyo, Japan.
Jpn J Exp Med. 1987 Jun;57(3):145-51.
The spinal cords in mice surviving acute infection for 30 days following lumbar inoculation with mouse hepatitis virus, JHM strain, were examined for virus growth and pathologic changes by light and electron microscopy. Virus titer reached a maximum level on day 6 postinoculation (p.i.) and became negative on day 10 p.i. On days 5 to 10 p.i. there were severe disruption of myelin sheath and marked phagocytosis of myelin by macrophages. Viral particles were seen in degenerating glial cells. On days 15 to 20 p.i. proliferation of oligodendrocytes was noticed in association with thinly myelinated axons with decreased number of macrophages. On days 25 to 30 p.i. affected axons were mostly remyelinated by oligodendrocytes and the interaxonal space was packed with the processes of fibrous astrocytes containing myelin debris and lipid droplets. In the subpial areas of more widespread lesions some axons were remyelinated by Schwann cells.
对经腰椎接种小鼠肝炎病毒JHM株后急性感染存活30天的小鼠脊髓,通过光学显微镜和电子显微镜检查病毒生长及病理变化。接种后第6天病毒滴度达到最高水平,接种后第10天转为阴性。接种后第5至10天,髓鞘严重破坏,巨噬细胞对髓鞘有明显吞噬作用。在变性的神经胶质细胞中可见病毒颗粒。接种后第15至20天,观察到少突胶质细胞增生,伴有髓鞘变薄的轴突,巨噬细胞数量减少。接种后第25至30天,受影响的轴突大多由少突胶质细胞重新髓鞘化,轴突间间隙充满含有髓鞘碎片和脂滴的纤维星形胶质细胞突起。在病变更广泛的软膜下区域,一些轴突由施万细胞重新髓鞘化。