Hepatitis C virus infection increases autophagosome stability by suppressing lysosomal fusion through an Arl8b-dependent mechanism.
Arl8b
GTPase
Hepatitis C virus (HCV)
autophagy
intracellular trafficking
lysosome
Journal
The Journal of biological chemistry
ISSN: 1083-351X
Titre abrégé: J Biol Chem
Pays: United States
ID NLM: 2985121R
Informations de publication
Date de publication:
27 09 2019
27 09 2019
Historique:
received:
28
02
2019
revised:
22
07
2019
pubmed:
7
8
2019
medline:
19
5
2020
entrez:
7
8
2019
Statut:
ppublish
Résumé
Autophagy is a conserved cellular process involving intracellular membrane trafficking and degradation. Pathogens, including hepatitis C virus (HCV), often exploit this process to promote their own survival. The aim of this study was to determine the mechanism by which HCV increases steady-state autophagosome numbers while simultaneously inhibiting flux through the autophagic pathway. Using the lysosomal inhibitor bafilomycin A1, we showed that HCV-induced alterations in autophagy result from a blockage of autophagosome degradation rather than an increase in autophagosome generation. In HCV-infected cells, lysosome function was normal, but a tandem RFP-GFP-LC3 failed to reach the lysosome even under conditions that activate autophagy. Autophagosomes and lysosomes isolated from HCV-infected cells were able to fuse with each other normally
Identifiants
pubmed: 31383738
pii: S0021-9258(20)34986-3
doi: 10.1074/jbc.RA119.008229
pmc: PMC6768644
doi:
Substances chimiques
ARL8B protein, human
0
ADP-Ribosylation Factors
EC 3.6.5.2
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
14257-14266Subventions
Organisme : NIGMS NIH HHS
ID : P30 GM103326
Pays : United States
Organisme : NIGMS NIH HHS
ID : P30 GM118247
Pays : United States
Organisme : NIGMS NIH HHS
ID : P30 GM122731
Pays : United States
Informations de copyright
© 2019 Jones-Jamtgaard et al.
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