Interaction between ns1 and cellular mavs contributes to ns1 mitochondria targeting

Yeu Yang Tseng; Chih Ying Kuan; Masaki Mibayashi; Chi Jene Chen; Peter Palese; Randy A. Albrecht; Wei Li Hsu

doi:10.3390/v13101909

Interaction between ns1 and cellular mavs contributes to ns1 mitochondria targeting

Yeu Yang Tseng, Chih Ying Kuan, Masaki Mibayashi, Chi Jene Chen, Peter Palese, Randy A. Albrecht, Wei Li Hsu

Research output: Contribution to journal › Article › peer-review

4 Scopus citations

Abstract

Influenza A virus nonstructural protein 1 (NS1) plays an important role in evading host innate immunity. NS1 inhibits interferon (IFN) responses via multiple mechanisms, including sequestering dsRNA and suppressing retinoic acid-inducible gene I (RIG-I) signaling by interacting with RIG-I and tripartite motif-containing protein 25 (TRIM25). In the current study, we demonstrated the mitochondrial localization of NS1 at the early stage of influenza virus infection. Since NS1 does not contain mitochondria-targeting signals, we suspected that there is an association between the NS1 and mitochondrial proteins. This hypothesis was tested by demonstrating the interaction of NS1 with mitochondrial antiviral-signaling protein (MAVS) in a RIG-I-independent manner. Importantly, the association with MAVS facilitated the mitochondrial localization of NS1 and thereby significantly impeded MAVS-mediated Type I IFN production.

Original language	English
Article number	1909
Journal	Viruses
Volume	13
Issue number	10
DOIs	https://doi.org/10.3390/v13101909
State	Published - Oct 2021

Keywords

Influenza A virus
MAVS
Mitochondria
NS1

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10.3390/v13101909

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title = "Interaction between ns1 and cellular mavs contributes to ns1 mitochondria targeting",

abstract = "Influenza A virus nonstructural protein 1 (NS1) plays an important role in evading host innate immunity. NS1 inhibits interferon (IFN) responses via multiple mechanisms, including sequestering dsRNA and suppressing retinoic acid-inducible gene I (RIG-I) signaling by interacting with RIG-I and tripartite motif-containing protein 25 (TRIM25). In the current study, we demonstrated the mitochondrial localization of NS1 at the early stage of influenza virus infection. Since NS1 does not contain mitochondria-targeting signals, we suspected that there is an association between the NS1 and mitochondrial proteins. This hypothesis was tested by demonstrating the interaction of NS1 with mitochondrial antiviral-signaling protein (MAVS) in a RIG-I-independent manner. Importantly, the association with MAVS facilitated the mitochondrial localization of NS1 and thereby significantly impeded MAVS-mediated Type I IFN production.",

keywords = "Influenza A virus, MAVS, Mitochondria, NS1",

author = "Tseng, {Yeu Yang} and Kuan, {Chih Ying} and Masaki Mibayashi and Chen, {Chi Jene} and Peter Palese and Albrecht, {Randy A.} and Hsu, {Wei Li}",

note = "Publisher Copyright: {\textcopyright} 2021 by the authors. Licensee MDPI, Basel, Switzerland.",

year = "2021",

month = oct,

doi = "10.3390/v13101909",

language = "English",

volume = "13",

journal = "Viruses",

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AU - Tseng, Yeu Yang

AU - Kuan, Chih Ying

AU - Mibayashi, Masaki

AU - Chen, Chi Jene

AU - Palese, Peter

AU - Albrecht, Randy A.

AU - Hsu, Wei Li

PY - 2021/10

Y1 - 2021/10

N2 - Influenza A virus nonstructural protein 1 (NS1) plays an important role in evading host innate immunity. NS1 inhibits interferon (IFN) responses via multiple mechanisms, including sequestering dsRNA and suppressing retinoic acid-inducible gene I (RIG-I) signaling by interacting with RIG-I and tripartite motif-containing protein 25 (TRIM25). In the current study, we demonstrated the mitochondrial localization of NS1 at the early stage of influenza virus infection. Since NS1 does not contain mitochondria-targeting signals, we suspected that there is an association between the NS1 and mitochondrial proteins. This hypothesis was tested by demonstrating the interaction of NS1 with mitochondrial antiviral-signaling protein (MAVS) in a RIG-I-independent manner. Importantly, the association with MAVS facilitated the mitochondrial localization of NS1 and thereby significantly impeded MAVS-mediated Type I IFN production.

AB - Influenza A virus nonstructural protein 1 (NS1) plays an important role in evading host innate immunity. NS1 inhibits interferon (IFN) responses via multiple mechanisms, including sequestering dsRNA and suppressing retinoic acid-inducible gene I (RIG-I) signaling by interacting with RIG-I and tripartite motif-containing protein 25 (TRIM25). In the current study, we demonstrated the mitochondrial localization of NS1 at the early stage of influenza virus infection. Since NS1 does not contain mitochondria-targeting signals, we suspected that there is an association between the NS1 and mitochondrial proteins. This hypothesis was tested by demonstrating the interaction of NS1 with mitochondrial antiviral-signaling protein (MAVS) in a RIG-I-independent manner. Importantly, the association with MAVS facilitated the mitochondrial localization of NS1 and thereby significantly impeded MAVS-mediated Type I IFN production.

KW - Influenza A virus

KW - MAVS

KW - Mitochondria

KW - NS1

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JO - Viruses

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M1 - 1909

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Interaction between ns1 and cellular mavs contributes to ns1 mitochondria targeting

Abstract

Keywords

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