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感染脑心肌炎病毒的哺乳动物背根神经节培养物中的脱髓鞘和细胞病变效应

Demyelination and cytopathic effects in cultures of mammalian dorsal root ganglia infected with encephalomyocarditis virus.

作者信息

Oren R, Shahar A, Monzain R

出版信息

J Virol. 1975 Aug;16(2):356-65. doi: 10.1128/JVI.16.2.356-365.1975.

Abstract

Replication of encephalomyocarditis virus and its cytopathic effects were studied in myelinated cultures of dorsal root ganglia obtained from newborn mice. Six hours after infection virus progeny was detected in the culture. At 24 h the virus titer reached 2 times 10(6) PFU per culture and remained at this level until 48 h. The first cytopathic alterations began at 24 h and consisted of rounding of Schwann and satellites cells and their detachment from neurons. Later, bead-like swellings of the myelin appeared along the axons followed by splitting and degeneration of lamellae. The cytopathic effect in the neurons started 29 h after infection, reaching complete neuronolysis at 48 h. Virus particles, scattered or arranged in crystal-like aggregates, were first seen in the cytoplasm of glial cells and then in neurons and axons.

摘要

在从新生小鼠获得的背根神经节有髓培养物中研究了脑心肌炎病毒的复制及其细胞病变效应。感染后6小时在培养物中检测到病毒子代。24小时时病毒滴度达到每培养物2×10⁶ PFU,并保持在该水平直至48小时。最初的细胞病变改变始于24小时,表现为施万细胞和卫星细胞变圆并与神经元分离。随后,沿轴突出现髓鞘的串珠样肿胀,接着是板层的分裂和变性。神经元中的细胞病变效应在感染后29小时开始,48小时时达到完全神经元溶解。病毒颗粒,分散或呈晶体样聚集排列,首先出现在神经胶质细胞的细胞质中,然后出现在神经元和轴突中。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6050/354675/26670824c921/jvirol00236-0152-a.jpg

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