2014年8月
Influenza A virus protein PB1-F2 translocates into mitochondria via Tom40 channels and impairs innate immunity
NATURE COMMUNICATIONS
ダウンロード
回数 : 288
- ,
- ,
- ,
- ,
- ,
- ,
- 巻
- 5
- 号
- 開始ページ
- 4713
- 終了ページ
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1038/ncomms5713
- 出版者・発行元
- NATURE PUBLISHING GROUP
Mitochondria contribute to cellular innate immunity against RNA viruses. Mitochondrial-mediated innate immunity is regulated by signalling molecules that are recruited to the mitochondrial membrane, and depends on the mitochondrial inner membrane potential (Delta psi(m)). Here we examine the physiological relevance of Delta psi(m) and the mitochondrial-associating influenza A viral protein PB1-F2 in innate immunity. When expressed in host cells, PB1-F2 completely translocates into the mitochondrial inner membrane space via Tom40 channels, and its accumulation accelerates mitochondrial fragmentation due to reduced Delta psi(m). By contrast, PB1-F2 variants lacking a C-terminal polypeptide, which is frequently found in low pathogenic subtypes, do not affect mitochondrial function. PB1-F2-mediated attenuation of Delta psi(m) suppresses the RIG-I signalling pathway and activation of NLRP3 inflammasomes. PB1-F2 translocation into mitochondria strongly correlates with impaired cellular innate immunity, making this translocation event a potential therapeutic target.
- リンク情報
- ID情報
-
- DOI : 10.1038/ncomms5713
- ISSN : 2041-1723
- Web of Science ID : WOS:000341079100002