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对由持续感染细胞培养物中的麻疹病毒引起的仓鼠亚急性脑炎和脑积水的进一步研究。

Further studies on subacute encephalitis and hydrocephalus in hamsters caused by measles virus from persistently infected cell cultures.

作者信息

Norrby E, Swoveland P, Kristensson K, Johnson K P

出版信息

J Med Virol. 1980;5(2):109-16. doi: 10.1002/jmv.1890050203.

DOI:10.1002/jmv.1890050203
PMID:7373285
Abstract

Newborn hamsters were inoculated intracerebrally (IC) with disrupted measles carrier Lu 106 cells. No acute neurological disease developed, but limited, persistent neural infection was identified by immune fluorescence and by virus isolation. By ten days after inoculation, virus could be recovered only by cocultivation of explant cultures of central nervous system (CNS) tissue and Vero cells. Virus was still demonstrable in CNS by both techniques 50 days after inoculation, the latest sample collected. Animals inoculated as newborns developed a poor hemagglutination-inhibiting (HI) antibody response. In three-week-old hamsters inoculated IC no detectable replication of carrier virus occurred. The serum HI antibody response was more than 20 times higher than that in animals inoculated as newborns. Hydrocephalus developed in a fraction of animals inoculated at birth or at the age of three weeks. Both infectious and heat-inactivated disrupted virus carrier material, but not control material of Lu 106 cells, gave hydrocephalus. The precise mechanism leading to hydrocephalus is unclear. Carrier virus material may produce a meningeal irritation causing disturbances of the extraventricular flow or resorption of cerebrospinal fluid, leading to communicating hydrocephalus. Infectious carrier virus may replicate in and destroy ependymal cells, further contributing to hydrocephalus.

摘要

将麻疹载体Lu 106细胞破碎后对新生仓鼠进行脑内接种(IC)。未出现急性神经疾病,但通过免疫荧光和病毒分离鉴定出存在局限性、持续性神经感染。接种后十天,只有通过中枢神经系统(CNS)组织外植体培养物与Vero细胞共培养才能回收病毒。在接种后50天(收集的最晚样本),两种技术仍可在中枢神经系统中检测到病毒。新生时接种的动物产生的血凝抑制(HI)抗体反应较差。对三周龄仓鼠进行脑内接种后,未检测到载体病毒的复制。血清HI抗体反应比新生时接种的动物高20倍以上。一部分出生时或三周龄时接种的动物出现了脑积水。有感染性的和热灭活的破碎病毒载体材料,但不是Lu 106细胞的对照材料,都会导致脑积水。导致脑积水的确切机制尚不清楚。载体病毒材料可能会引起脑膜刺激,导致脑室外流或脑脊液吸收紊乱,从而导致交通性脑积水。有感染性的载体病毒可能会在室管膜细胞中复制并将其破坏,进一步导致脑积水。

相似文献

1
Further studies on subacute encephalitis and hydrocephalus in hamsters caused by measles virus from persistently infected cell cultures.对由持续感染细胞培养物中的麻疹病毒引起的仓鼠亚急性脑炎和脑积水的进一步研究。
J Med Virol. 1980;5(2):109-16. doi: 10.1002/jmv.1890050203.
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Subacute encephalitis and hydrocephalus in hamsters caused by measles virus from persistently infected cell cultures.由持续感染细胞培养物中的麻疹病毒引起的仓鼠亚急性脑炎和脑积水。
J Med Virol. 1978;2(4):305-17. doi: 10.1002/jmv.1890020404.
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Encephalitis after inhalation of measles virus: a pathogenetic study in hamsters.吸入麻疹病毒后的脑炎:仓鼠的发病机制研究
Ann Neurol. 1981 Jan;9(1):21-7. doi: 10.1002/ana.410090105.
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Potentiation of experimental allergic encephalomyelitis in hamsters with persistent encephalitis due to measles virus.
J Infect Dis. 1979 Mar;139(3):297-303. doi: 10.1093/infdis/139.3.297.

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J Virol. 2000 Sep;74(17):7972-9. doi: 10.1128/jvi.74.17.7972-7979.2000.
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The H gene of rodent brain-adapted measles virus confers neurovirulence to the Edmonston vaccine strain.啮齿动物脑适应性麻疹病毒的H基因赋予了埃德蒙斯顿疫苗株神经毒力。
J Virol. 1999 Aug;73(8):6916-22. doi: 10.1128/JVI.73.8.6916-6922.1999.