PIAS1 Regulates Hepatitis C Virus-Induced Lipid Droplet Accumulation by Controlling Septin 9 and Microtubule Filament Assembly.
HCV
PIAS1
lipid droplets
septin 9
Journal
Pathogens (Basel, Switzerland)
ISSN: 2076-0817
Titre abrégé: Pathogens
Pays: Switzerland
ID NLM: 101596317
Informations de publication
Date de publication:
15 Oct 2021
15 Oct 2021
Historique:
received:
07
09
2021
revised:
07
10
2021
accepted:
13
10
2021
entrez:
23
10
2021
pubmed:
24
10
2021
medline:
24
10
2021
Statut:
epublish
Résumé
Chronic hepatitis C virus (HCV) infection often leads to fibrosis and chronic hepatitis, then cirrhosis and ultimately hepatocellular carcinoma (HCC). The processes of the HVC life cycle involve intimate interactions between viral and host cell proteins and lipid metabolism. However, the molecules and mechanisms involved in this tripartite interaction remain poorly understood. Herein, we show that the infection of HCC-derived Huh7.5 cells with HCV promotes upregulation of the protein inhibitor of activated STAT1 (PIAS1). Reciprocally, PIAS1 regulated the expression of HCV core protein and HCV-induced LD accumulation and impaired HCV replication. Furthermore, PIAS1 controlled HCV-promoted septin 9 filament formation and microtubule polymerization. Subsequently, we found that PIAS1 interacted with septin 9 and controlled its assembly on filaments, which thus affected septin 9-induced lipid droplet accumulation. Taken together, these data reveal that PIAS1 regulates the accumulation of lipid droplets and offer a meaningful insight into how HCV interacts with host proteins.
Identifiants
pubmed: 34684276
pii: pathogens10101327
doi: 10.3390/pathogens10101327
pmc: PMC8537804
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : ANRS and Association pour la Recherche sur le Cancer
ID : ARC/SUBV/CKLQ6
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