Transgenic mice expressing human measles virus (MV) receptor CD46 provide cells exhibiting different permissivities to MV infection
Transgenic mice expressing human measles virus (MV) receptor CD46 provide cells exhibiting different permissivities to MV infection
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DOI：
10.1128/jvi.70.10.6673-6681.1996
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发表时间：
1996-10-01
影响因子：
5.4
通讯作者：
RabourdinCombe, C
中科院分区：
文献类型：
--
作者：
Horvat, B;Rivailler, P;RabourdinCombe, C
我们已经产生了普遍表达麻疹病毒（MV）的人受体CD 46的转基因小鼠从这些转基因小鼠中分离各种细胞类型，分析它们在体外支持MV复制的能力。尽管MV可以进入所有表达CD 46的细胞，但根据细胞类型检测到对MV感染的不同易感性，从转基因小鼠肺和肾中分离的细胞培养物被发现允许MV感染，因为检测到MV基因特异性RNA并释放病毒颗粒，尽管在低水平。类似于人淋巴细胞，从转基因小鼠分离的活化的T和B淋巴细胞可以支持MV复制;当表达病毒蛋白时，淋巴细胞从表面下调CD 46。有趣的是，虽然来自非转基因小鼠的活化的T淋巴细胞不支持MV感染，但活化的非转基因小鼠B淋巴细胞复制MV以及转基因B淋巴细胞，这表明使用替代病毒受体进入。与先前的细胞类型相反，鼠腹膜和骨髓来源的巨噬细胞，无论它们是否被激活，都不能支持MV复制。此外，虽然MV进入巨噬细胞并发生病毒特异性RNA转录，但未检测到病毒蛋白或感染性病毒颗粒。这些结果表明，特定的细胞类型特异性宿主因子对MV在小鼠细胞中复制的重要性，这可能是MV感染的差异性传播的原因。
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.