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通过原位杂交检测小鼠肝炎病毒A59 RNA在小鼠慢病毒脱髓鞘感染中的持续存在情况。

Persistence of mouse hepatitis virus A59 RNA in a slow virus demyelinating infection in mice as detected by in situ hybridization.

作者信息

Lavi E, Gilden D H, Highkin M K, Weiss S R

出版信息

J Virol. 1984 Aug;51(2):563-6. doi: 10.1128/JVI.51.2.563-566.1984.

Abstract

Mouse hepatitis virus strain A59 produces chronic central nervous system demyelination in rodents. As late as 6 months after intracerebral inoculation of mice 4 to 6 weeks old, when infectious virus cannot be recovered and viral antigens cannot be detected in the central nervous systems and livers of these animals, primary demyelination is still evident. Using cloned virus-specific DNAs and the highly sensitive and specific technique of in situ hybridization, we have detected low levels of mouse hepatitis virus A59 RNA in the central nervous systems and livers of mice 10 months after inoculation. We suggest that viral persistence may play a role in mouse hepatitis virus A59-induced chronic demyelination.

摘要

小鼠肝炎病毒A59株可在啮齿动物中引发慢性中枢神经系统脱髓鞘病变。在给4至6周龄的小鼠进行脑内接种后长达6个月时,尽管在这些动物的中枢神经系统和肝脏中无法检测到传染性病毒且检测不到病毒抗原,但原发性脱髓鞘病变仍然明显。利用克隆的病毒特异性DNA以及原位杂交这种高度灵敏且特异的技术,我们在接种后10个月的小鼠中枢神经系统和肝脏中检测到了低水平的小鼠肝炎病毒A59 RNA。我们认为病毒持续存在可能在小鼠肝炎病毒A59诱导的慢性脱髓鞘病变中发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74d4/254475/3d9756e530c2/jvirol00131-0306-a.jpg

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