論文

査読有り 筆頭著者 責任著者 本文へのリンクあり
2011年9月13日

Expression of the Sendai (murine parainfluenza) virus C protein alleviates restriction of measles virus growth in mouse cells

Proceedings of the National Academy of Sciences of the United States of America
  • Masaharu Iwasaki
  • ,
  • Yusuke Yanagi

108
37
開始ページ
15384
終了ページ
15389
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1073/pnas.1107382108
出版者・発行元
NATL ACAD SCIENCES

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 muchmore 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.

リンク情報
DOI
https://doi.org/10.1073/pnas.1107382108
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/21896767
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000294804900077&DestApp=WOS_CPL
Scopus
https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=80053075924&origin=inward 本文へのリンクあり
Scopus Citedby
https://www.scopus.com/inward/citedby.uri?partnerID=HzOxMe3b&scp=80053075924&origin=inward
ID情報
  • DOI : 10.1073/pnas.1107382108
  • ISSN : 0027-8424
  • eISSN : 1091-6490
  • PubMed ID : 21896767
  • SCOPUS ID : 80053075924
  • Web of Science ID : WOS:000294804900077

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