ATAD1 inhibits hepatitis C virus infection by removing the viral TA-protein NS5B from mitochondria.
hepatitis C virus infection
mitochondria
protein degradation
protein interaction
tail-anchored protein
Journal
EMBO reports
ISSN: 1469-3178
Titre abrégé: EMBO Rep
Pays: England
ID NLM: 100963049
Informations de publication
Date de publication:
06 11 2023
06 11 2023
Historique:
revised:
24
08
2023
received:
06
12
2022
accepted:
01
09
2023
pmc-release:
03
10
2024
medline:
7
11
2023
pubmed:
4
10
2023
entrez:
4
10
2023
Statut:
ppublish
Résumé
ATPase family AAA domain-containing protein 1 (ATAD1) maintains mitochondrial homeostasis by removing mislocalized tail-anchored (TA) proteins from the mitochondrial outer membrane (MOM). Hepatitis C virus (HCV) infection induces mitochondrial fragmentation, and viral NS5B protein is a TA protein. Here, we investigate whether ATAD1 plays a role in regulating HCV infection. We find that HCV infection has no effect on ATAD1 expression, but knockout of ATAD1 significantly enhances HCV infection; this enhancement is suppressed by ATAD1 complementation. NS5B partially localizes to mitochondria, dependent on its transmembrane domain (TMD), and induces mitochondrial fragmentation, which is further enhanced by ATAD1 knockout. ATAD1 interacts with NS5B, dependent on its three internal domains (TMD, pore-loop 1, and pore-loop 2), and induces the proteasomal degradation of NS5B. In addition, we provide evidence that ATAD1 augments the antiviral function of MAVS upon HCV infection. Taken together, we show that the mitochondrial quality control exerted by ATAD1 can be extended to a novel antiviral function through the extraction of the viral TA-protein NS5B from the mitochondrial outer membrane.
Identifiants
pubmed: 37789674
doi: 10.15252/embr.202256614
pmc: PMC10626439
doi:
Substances chimiques
Viral Proteins
0
Antiviral Agents
0
Viral Nonstructural Proteins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e56614Informations de copyright
© 2023 The Authors.
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