Cellular factors involved in the hepatitis C virus life cycle

Li, Huichun; Yang, Chee-Hing; Lo, Shih-Yen

doi:10.3748/wjg.v27.i28.4555

Cited by 14 publications

(14 citation statements)

References 322 publications

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“…LDs play a crucial role in the HCV life cycle and, in most cases, interactions between HCV proteins (particularly the HCV core protein) and LDs are required for morphogenesis and the production of infectious HCV [ 55 , 60 ]. Although hundreds of cellular factors have been identified as being involved in the HCV life cycle [ 61 ], how they contribute to HCV pathogenesis remains unknown.…”

Section: Discussionmentioning

confidence: 99%

PIAS1 Regulates Hepatitis C Virus-Induced Lipid Droplet Accumulation by Controlling Septin 9 and Microtubule Filament Assembly

et al. 2021

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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.

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Section: Discussionmentioning

confidence: 99%

PIAS1 Regulates Hepatitis C Virus-Induced Lipid Droplet Accumulation by Controlling Septin 9 and Microtubule Filament Assembly

et al. 2021

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“…3 ). Hierzu gehören der „low density lipoprotein receptor“ (LDLR), die Heparansulfat-Proteoglykane (HSPG), der „scavenger receptor class B type 1“ (SR-B1), das Tetraspanin CD81, Claudin 1 (CLDN1) und Occludin (OCLN), der Cholesteroltransporter Niemann-Pick C1-like (NPC1L1), die Rezeptortyrosinkinasen „epidermal growth factor receptor“ (EGFR) und „ephidrin type A receptor 2“ (EPHA2) sowie der Transferrinrezeptor (TfR; eine aktuelle Übersicht findet sich in [ 49 , 50 ]). Nach clathrin-abhängiger Endozytose wird das RNA-Genom pH-abhängig in das Zytoplasma der Zelle freigesetzt, wo es als mRNA-Template für die Synthese des HCV-Polyproteins dient.…”

Section: Das Hepatitis-c-virusunclassified

Die Virushepatitiden A bis E: Prävalenz, Erregermerkmale und Pathogenese

Bender

Glitscher

Hildt

2021

Bundesgesundheitsbl

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ZusammenfassungBei der viralen Hepatitis handelt es sich um eine akute oder chronische Entzündung der Leber, die durch verschiedene Viren verursacht wird. Weltweit leiden derzeit ca. 325 Mio. Menschen an der chronischen Form. Jährlich versterben insgesamt ca. 1,6 Mio. an den Folgen einer viralen Hepatitis. Die Hepatitisviren werden in 5 Erregergruppen unterteilt, die mit den Buchstaben A bis E bezeichnet werden (HAV–HEV). Diese unterscheiden sich in Phylogenie, Übertragung, Epidemiologie, Wirtsspezifität, Lebenszyklus, Struktur und in speziellen Aspekten der Pathogenese.Das strikt humanpathogene HAV, Teil der Familie Picornaviridae, induziert meist nur akute Hepatitiden und ist primär in Entwicklungsländern verbreitet. Das den Hepeviridae zugeordnete HEV beschreibt eine ähnliche Epidemiologie, ist jedoch durch sein zoonotisches Potenzial auch in Industrienationen weitverbreitet und kann zusätzlich eine chronische Erkrankung induzieren. Eine Chronifizierung tritt ebenso bei dem weltweit verbreiteten HBV (Hepadnaviridae) auf, dessen Satellitenvirus HDV (Kolmioviridae) das vorhandene kanzerogene Potenzial noch einmal erhöht. Das ebenfalls weltweit verbreitete HCV (Flaviviridae) birgt ein äußerst hohes Risiko der Chronifizierung und somit ebenfalls ein stark erhöhtes, kanzerogenes Potenzial.Die Erreger der viralen Hepatitis unterscheiden sich in ihren Eigenschaften und Lebenszyklen. Eine differenzierte Betrachtung im Hinblick auf Epidemiologie, Nachweismethoden und Prävention ist daher angezeigt. Obwohl robuste Therapien, und im Falle einzelner Erreger auch Vakzine, vorhanden sind, muss die Forschung insbesondere in Hinblick auf die armutsassoziierten Erreger erheblich vorangetrieben werden.

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“…HCV interaction with CD81 I induces multiple downstream signaling pathways, including Rho GTPase family members, Cdc42, and mitogen-activated protein kinase pathways (Farquhar et al 2011 ). EFGR is a coenzyme that aids in developing the CD81-CLDN1 complex and upregulates several downstream molecules in preparation for HCV genetic material insertion (Li et al 2021 ). Characterization of CD81 is through four conserved cysteine residues, including a ubiquitous CCG motif, and two additional cysteines in the LEL, that form critical disulfide bonds in LEL.…”

Section: Introductionmentioning

confidence: 99%

Target-specificity of different amyrin subunits in impeding HCV influx mechanism inside the human cells considering the quantum tunnel profiles and molecular strings of the CD81 receptor: a combined in silico and in vivo study

Jabin

Uddin

Azad

et al. 2023

In Silico Pharmacol.

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HCV is a hepatotropic RNA virus recognized for its frequent virulence and fatality worldwide. Despite many vaccine development programs underway, researchers are on a quest for natural bioactive compounds due to their multivalent efficiencies against viral infections, considering which the current research aimed to figure out the target-specificity and therapeutic potentiality of α, β, and δ subunits of amyrin, as novel bioactive components against the HCV influx mechanism. Initially, the novelty of amyrin subunits was conducted from 203 pharmacophores, comparing their in-silico pharmacokinetic and pharmacodynamic profiles. Besides, the best active site of CD81 was determined following the quantum tunneling algorithm. The molecular dynamic simulation was conducted (100 ns) following the molecular docking steps to reveal the parameters- RMSD (Å); Cα; RMSF (Å); MolSA (Å 2 ); Rg (nm); PSA (Å); SASA (Å 2 ), and the MM-GBSA dG binding scores. Besides, molecular strings of CD81, along with the co-expressed genes, were classified, as responsible for encoding CD81-mediated protein clusters during HCV infection, resulting in the potentiality of amyrins as targeted prophylactics in HCV infection. Finally, in vivo profiling of the oxidative stress marker, liver-specific enzymes, and antioxidant markers was conducted in the DMN-induced mice model, where β -amyrin scored the most significant values in all aspects.

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Cellular factors involved in the hepatitis C virus life cycle

Cited by 14 publications

References 322 publications

PIAS1 Regulates Hepatitis C Virus-Induced Lipid Droplet Accumulation by Controlling Septin 9 and Microtubule Filament Assembly

PIAS1 Regulates Hepatitis C Virus-Induced Lipid Droplet Accumulation by Controlling Septin 9 and Microtubule Filament Assembly

Die Virushepatitiden A bis E: Prävalenz, Erregermerkmale und Pathogenese

Target-specificity of different amyrin subunits in impeding HCV influx mechanism inside the human cells considering the quantum tunnel profiles and molecular strings of the CD81 receptor: a combined in silico and in vivo study

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