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小鼠肝炎病毒的温度敏感突变体导致脱髓鞘的发生率很高。

Temperature-sensitive mutants of mouse hepatitis virus produce a high incidence of demyelination.

作者信息

Haspel M V, Lampert P W, Oldstone M B

出版信息

Proc Natl Acad Sci U S A. 1978 Aug;75(8):4033-6. doi: 10.1073/pnas.75.8.4033.

DOI:10.1073/pnas.75.8.4033
PMID:279022
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC392925/
Abstract

Mutagenesis of mouse hepatitis virus with 5-azacytidine or 5-fluorouracil yielded several temperature-sensitive mutants. Mutants have been isolated that dramatically enhance the production of demyelinating disease over that previously noted with the wild-type virus. This reproducible model should now make possible the precise elucidation of the pathogenic mechanism and molecular basis of this virus-induced demyelination.

摘要

用5-氮杂胞苷或5-氟尿嘧啶对小鼠肝炎病毒进行诱变产生了几个温度敏感突变体。已分离出的突变体显著增强了脱髓鞘疾病的产生，超过了先前野生型病毒所引起的程度。这种可重复的模型现在应该能够精确阐明这种病毒诱导脱髓鞘的致病机制和分子基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f561/392925/4021e3da97a2/pnas00020-0504-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f561/392925/4021e3da97a2/pnas00020-0504-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f561/392925/4021e3da97a2/pnas00020-0504-a.jpg

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