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柯萨奇病毒对小鼠成纤维细胞的持续感染。

Persistent infection of mouse fibroblasts with Coxsackievirus.

作者信息

Schnurr D P, Schmidt N J

出版信息

Arch Virol. 1984;81(1-2):91-101. doi: 10.1007/BF01309299.

Abstract

Infection of fibroblast cell lines initiated from BALB/c or NFR mice with coxsackievirus B3 (CBV-3) or B4 (CBV-4) resulted in infections which persisted for a limited number of subpassages of the infected cells in most cases, but for over a year in one case. In all instances primary acute infections were characterized by cytopathology and release of infectious virus progeny. Viral antigen could be detected during the acute phase of infection, but not in subcultured infected cells. Infectious center assays showed that every cell was infected during the acute phase of infection, but that from the first subcultivation on, the numbers of cells which were able to initiate infection were greatly reduced. The long term persistent CBV-3 infection was characterized by wide fluctuations in titers of virus released into the supernatant fluids. Interferon did not appear to play a role in maintenance of the persistent infection. Information derived from studies on mechanisms of CBV persistence in the in vitro model may help to elucidate the role of CBV in chronic human diseases such as myocarditis.

摘要

用柯萨奇病毒B3(CBV-3)或B4(CBV-4)感染源自BALB/c或NFR小鼠的成纤维细胞系,在大多数情况下,感染在受感染细胞传代培养有限次数后就会持续,但有一例持续了一年多。在所有情况下,原发性急性感染的特征是细胞病理学变化和感染性病毒子代的释放。在感染急性期可检测到病毒抗原,但在传代培养的受感染细胞中则检测不到。感染中心试验表明,在感染急性期每个细胞都被感染,但从第一次传代培养开始,能够引发感染的细胞数量就大大减少。长期持续的CBV-3感染的特征是释放到上清液中的病毒滴度有很大波动。干扰素似乎在维持持续感染中不起作用。从体外模型中关于CBV持续存在机制的研究中获得的信息可能有助于阐明CBV在诸如心肌炎等慢性人类疾病中的作用。

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