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• W2136516768 abstract "Measles virus (MV), a human pathogen, uses the signaling lymphocyte activation molecule (SLAM) or CD46 as an entry receptor. Although several transgenic mice expressing these receptors have been generated as small animal models for measles, these mice usually have to be made defective in IFN-α/β signaling to facilitate MV replication. Similarly, when functional receptors are expressed by transfection, mouse cells do not allow MV growth as efficiently as primate cells. In this study, we demonstrate that MV efficiently grows in SLAM-expressing mouse cells in which the Sendai virus (SeV) C protein is transiently expressed. We developed a SLAM-expressing mouse cell line whose genome also encodes the SeV C protein downstream of the sequence flanked with loxP sequences. When this cell line was infected with the recombinant MV expressing the Cre recombinase, the SeV C protein was readily expressed. Importantly, the Cre recombinase-encoding MV grew in this cell line much more efficiently than it did in the parental cell. The minigenome assay demonstrated that the SeV C protein does not modulate MV RNA synthesis. Analyses using the mutant proteins with the defined functional defects revealed that the IFN-antagonist function, but not the budding-accelerating function, of the SeV C protein was critical for supporting efficient MV growth in mouse cells. Our results indicate that insufficient IFN antagonism can be an important determinant of the host range of viruses, and the system described here may be useful to overcome the species barrier of other human viruses." @default.
• W2136516768 created "2016-06-24" @default.
• W2136516768 creator A5039422869 @default.
• W2136516768 creator A5078312528 @default.
• W2136516768 date "2011-09-01" @default.
• W2136516768 modified "2023-09-26" @default.
• W2136516768 title "Expression of the Sendai (murine parainfluenza) virus C protein alleviates restriction of measles virus growth in mouse cells" @default.
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• W2136516768 doi "https://doi.org/10.1073/pnas.1107382108" @default.
• W2136516768 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3174579" @default.
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• W2136516768 hasPublicationYear "2011" @default.
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