Transgenic mice expressing human measles virus (MV) receptor CD46 provide cells exhibiting different permissivities to MV infection

被引:100
作者
Horvat, B [1 ]
Rivailler, P [1 ]
VariorKrishnan, G [1 ]
Cardoso, A [1 ]
Gerlier, D [1 ]
RabourdinCombe, C [1 ]
机构
[1] FAC MED LYON LAENNEC,CNRS,IVMC,UCBL UMR 5537,F-69372 LYON,FRANCE
关键词
D O I
10.1128/JVI.70.10.6673-6681.1996
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
We have generated transgenic mice ubiquitously expressing the human receptor for measles virus (MV), CD46 (membrane cofactor protein), Various cell types were isolated from these transgenic mice acid analyzed for their ability to support MV replication in vitro, Although MV could enter into all CD46-expressing cells, differential susceptibilities to MV infection were detected depending on the cell type, Cell cultures obtained from transgenic lungs and kidneys were found to be permissive of MV infection, since RNA specific for MV genes was detected and viral particles were released, although at a low level, Similarly to human lymphocytes, activated T and B lymphocytes isolated from transgenic mice could support MV replication; virus could enter, transcribe viral RNA, and produce new infectious particles, When expressing viral proteins, lymphocytes down-regulated CD46 from the surface, Interestingly, while activated T lymphocytes from nontransgenic mice did not support MV infection, activated nontransgenic murine B Lymphocytes replicated MV as well as transgenic B lymphocytes, suggesting the use of an alternative virus receptor for entry. In contrast to the previous cell types, murine peritoneal and bone marrow derived macrophages, regardless of whether they were activated, could not support MV replication. Furthermore, although MV entered into macrophages and virus-specific RNA transcription occurred, no virus protein or infectious virus particles could be detected, These results show the importance of the particular cell-type-specific host factors for MV replication in murine cells which may be responsible for the differential permissivity of MV infection.
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页码:6673 / 6681
页数:9
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