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小鼠冠状病毒SD的发病机制。I. 在无传染性病毒产生情况下的显著脱髓鞘。

Pathogenesis of coronavirus SD in mice. I. Prominent demyelination in the absence of infectious virus production.

作者信息

Mendelman P M, Jankovsky L D, Murray R S, Licari P, DeVald B, Gerdes J C, Burks J S

出版信息

Arch Neurol. 1983 Aug;40(8):493-8. doi: 10.1001/archneur.1983.04210070033010.

DOI:10.1001/archneur.1983.04210070033010
PMID:6870610
Abstract

Following intracerebral inoculation of 3- to 4-week-old C57 B16/J mice with coronavirus SD, 23% exhibited neurologic signs within the first week. However, only 6% died. Within the first week after inoculation (AI), we noted a panencephalitis. Prominent demyelination detected in the spinal cord on day 6 continued through day 29 AI. Demyelinated lesions in the spinal cord were either subpial with few inflammatory cells except for macrophages or perivascular with prominent accumulation of lymphocytes, plasma cells, and macrophages. Beginning on day 6 AI, IgG was detected in the lesions. Although an infectious virus was detectable in the CNS only through day 12 AI, viral antigen expression continued through day 24. We concluded that coronavirus SD persists in a nonrecoverable form throughout the initial phase of demyelination, day 6 to day 24 AI.

摘要

给3至4周龄的C57 B16/J小鼠脑内接种冠状病毒SD后,23%的小鼠在第一周内出现神经症状。然而,只有6%死亡。在接种后的第一周(AI),我们观察到全脑炎。在接种后第6天在脊髓中检测到的明显脱髓鞘持续至接种后第29天。脊髓中的脱髓鞘病变要么位于软膜下,除巨噬细胞外几乎没有炎症细胞,要么位于血管周围,有淋巴细胞、浆细胞和巨噬细胞的显著聚集。从接种后第6天开始,在病变中检测到IgG。尽管仅在接种后第12天之前可在中枢神经系统中检测到感染性病毒,但病毒抗原表达持续至接种后第24天。我们得出结论,冠状病毒SD在脱髓鞘的初始阶段(接种后第6天至第24天)以不可恢复的形式持续存在。

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