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携带H-2Db基因的转基因FVB小鼠对泰勒氏病毒的持续感染产生抗性。

FVB mice transgenic for the H-2Db gene become resistant to persistent infection by Theiler's virus.

作者信息

Azoulay A, Brahic M, Bureau J F

机构信息

Unité des Virus Lents, UA 1157 Centre National de la Recherche Scientifique, Institut Pasteur, Paris, France.

出版信息

J Virol. 1994 Jun;68(6):4049-52. doi: 10.1128/JVI.68.6.4049-4052.1994.

Abstract

The DA strain of Theiler's virus causes a persistent infection of the white matter of the spinal cord with chronic inflammation and primary demyelination. Inbred strains of mice differ greatly in their susceptibility to this disease. It has been shown that both viral persistence and demyelination are controlled mainly by a gene located in the H-2D region. This raised the possibility that the H-2D gene itself controls viral persistence, which in turn determines demyelination. In the present work we introduced the H-2Db gene of resistant C57BL/6 mice into the genome of susceptible H-2q FVB mice and showed that the FVB mice become resistant to persistence of the infection and did not develop inflammatory lesions.

摘要

泰勒氏病毒的DA株可导致脊髓白质的持续性感染,并伴有慢性炎症和原发性脱髓鞘。近交系小鼠对这种疾病的易感性差异很大。研究表明,病毒的持续性和脱髓鞘主要受位于H-2D区域的一个基因控制。这就提出了一种可能性,即H-2D基因本身控制病毒的持续性,而病毒的持续性又反过来决定脱髓鞘。在本研究中,我们将抗性C57BL/6小鼠的H-2Db基因导入易感的H-2q FVB小鼠的基因组中,结果显示FVB小鼠对感染的持续性产生抗性,且未出现炎性病变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8bc8/236915/af0e9fb75a90/jvirol00015-0608-a.jpg

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