Influenza A virus protein PB1-F2 translocates into mitochondria via Tom40 channels and impairs innate immunity

Takuma Yoshizumi, Takeshi Ichinohe, Osamu Sasaki, Hidenori Otera, Shun-ichiro Kawabata, Katsuyoshi Mihara and Takumi Koshiba ()
Additional contact information
Takuma Yoshizumi: Faculty of Sciences, Kyushu University
Takeshi Ichinohe: International Research Center for Infectious Diseases, Institute of Medical Science, The University of Tokyo
Osamu Sasaki: Faculty of Sciences, Kyushu University
Hidenori Otera: Graduate School of Medical Science, Kyushu University
Shun-ichiro Kawabata: Faculty of Sciences, Kyushu University
Katsuyoshi Mihara: Graduate School of Medical Science, Kyushu University
Takumi Koshiba: Faculty of Sciences, Kyushu University

Nature Communications, 2014, vol. 5, issue 1, 1-14

Abstract: Abstract 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 (Δψm). Here we examine the physiological relevance of Δψm 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 Δψm. 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 Δψm 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.

Date: 2014
References: Add references at CitEc
Citations: View citations in EconPapers (2)

Downloads: (external link)
https://www.nature.com/articles/ncomms5713 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5713

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms5713

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().