scholarly journals Lipid Droplet Binding of Hepatitis C Virus Core Protein Genotype 3

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Guan Qiang ◽  
Ravi Jhaveri
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Lipid Droplet ◽  
Lipid Droplets ◽  
Fluorescent Protein ◽  
Core Protein ◽  
Genotype 1 ◽  
Genotype 3 ◽  
Core Domain ◽  
Domain 3

Background. Hepatitis C virus (HCV) genotype 3 is known to cause steatosis (fatty liver) that is more frequent and severe than other genotypes. We previously identified sequence elements within genotype 3 HCV Core domain 3 that were sufficient for lipid accumulation. Aims. We examined various genotype 3 Core domains for lipid droplet localization and compared the lipid droplet binding regions of domain 2 with a genotype 1 isolate. Methods. We generated HCV Core domain constructs fused with green fluorescent protein and performed immunofluorescence to visualize lipid droplets. Results. Constructs containing HCV Core domain 2 are appropriately localized to lipid droplets with varying degrees of efficiency. When compared to genotype 1, there are polymorphisms within domain 2 that do not appear to alter lipid droplet localization. Conclusions. In summary, the differences in a steatosis-associated HCV Core genotype 3 isolate do not appear to involve altered lipid droplet localization.

scholarly journals Disrupting the association of hepatitis C virus core protein with lipid droplets correlates with a loss in production of infectious virus

2007 ◽  
Vol 88 (8) ◽  
pp. 2204-2213 ◽  
Author(s):  
Steeve Boulant ◽  
Paul Targett-Adams ◽  
John McLauchlan
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Lipid Droplet ◽  
Lipid Droplets ◽  
Core Protein ◽  
Virus Production ◽  
Endoplasmic Reticulum Membrane ◽  
Wild Type ◽  
The Core ◽  
Phenylalanine Residue

In infected cells, hepatitis C virus (HCV) core protein is targeted to lipid droplets, which serve as intracellular storage organelles. Using a tissue culture system to generate infectious HCV, we have shown that the coating of lipid droplets by the core protein occurs in a time-dependent manner and coincides with higher rates of virus production. At earlier times, the protein was located at punctate sites in close proximity to the edge of lipid droplets. Investigations by using Z-stack analysis have shown that many lipid droplets contained a single punctate site that could represent positions where core transfers from the endoplasmic reticulum membrane to droplets. The effects of lipid droplet association on virus production were studied by introducing mutations into the domain D2, the C-terminal region of the core protein necessary for droplet attachment. Alteration of a phenylalanine residue that was crucial for lipid droplet association generated an unstable form of the protein that could only be detected in the presence of a proteasome inhibitor. Moreover, converting two proline residues in D2 to alanines blocked coating of lipid droplets by core, although the protein was directed to punctate sites that were indistinguishable from those observed at early times for wild-type core protein. Neither of these virus mutants gave rise to virus progeny. By contrast, mutation at a cysteine residue positioned 2 aa upstream of the phenylalanine residue did not affect lipid droplet localization and produced wild-type levels of infectious progeny. Taken together, our findings indicate that lipid droplet association by core is connected to virus production.

scholarly journals Ultrastructural and quantitative analysis of the lipid droplet clustering induced by hepatitis C virus core protein

2010 ◽  
Vol 67 (18) ◽  
pp. 3151-3161 ◽  
Author(s):  
Marion Depla ◽  
Rustem Uzbekov ◽  
Christophe Hourioux ◽  
Emmanuelle Blanchard ◽  
Amélie Le Gouge ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Quantitative Analysis ◽  
Hepatitis C ◽  
Lipid Droplet ◽  
Core Protein ◽  
Virus Core

scholarly journals Hepatitis C Virus Core Protein Induces Lipid Droplet Redistribution in a Microtubule- and Dynein-Dependent Manner

Traffic ◽  
2008 ◽  
Vol 9 (8) ◽  
pp. 1268-1282 ◽  
Author(s):  
Steeve Boulant ◽  
Mark W. Douglas ◽  
Laura Moody ◽  
Agata Budkowska ◽  
Paul Targett-Adams ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Lipid Droplet ◽  
Core Protein ◽  
Dependent Manner ◽  
Virus Core

773 HEPATITIS C VIRUS AND LIPID DROPLETS: ROLE OF SEIPIN IN LIPID DROPLET MATURATION AND VIRAL LIFE CYCLE

2011 ◽  
Vol 54 ◽  
pp. S311 ◽  
Author(s):  
S. Clement ◽  
C. Fauvelle ◽  
S. Pascarella ◽  
S. Conzelmann ◽  
V. Kaddai ◽  
...  
Keyword(s):  
Life Cycle ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Lipid Droplet ◽  
Lipid Droplets ◽  
Viral Life Cycle

scholarly journals ‘Distribution of Hepatitis C Virus genotypes in northern Greece in the last decade: descriptive analysis and clinical correlations’

2019 ◽  
Vol 4 ◽  
Author(s):  
G. Gioula ◽  
E. Sinakos ◽  
E. Gigi ◽  
I. Goulis ◽  
T. Vasiliadis ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Drug Use ◽  
Intravenous Drug ◽  
Genotype Distribution ◽  
Intravenous Drug Use ◽  
Genotype 1 ◽  
Genotype 3 ◽  
Northern Greece ◽  
Hcv Genotype

Abstract Hepatitis C virus (HCV) represents a major public health problem, while the identification of a HCV genotype is clinically very important for therapy prescription. The aim of the present study was to determine the HCV genotype distribution patients from northern Greece with HCV RNA positive viral load and to identify whether there is a shift in this distribution, during 2009–2017. The study was performed on 915 HCV positive patients and according to the results, genotype 3 was the most prevalent genotype (Ν = 395, 43.2%) followed by genotype 1 (Ν = 361, 39.5%). Regarding the gender of the patients, genotype 1 was mostly detected in women. Moreover, genotype 1 was associated with higher viral loads, while genotype 3 was most frequently detected in patients with a history of intravenous drug use. In conclusion, our results show that genotype 3 is the most prevalent genotype in Greece during the last decade as opposed to older epidemiological studies, likely due to intravenous drug use becoming the major source of infection.

scholarly journals The genotype 3-specific hepatitis C virus core protein residue phenylalanine 164 increases steatosis in an in vitro cellular model

Gut ◽  
2007 ◽  
Vol 56 (9) ◽  
pp. 1302-1308 ◽  
Author(s):  
C Hourioux ◽  
R Patient ◽  
A Morin ◽  
E Blanchard ◽  
A Moreau ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Core Protein ◽  
Cellular Model ◽  
Genotype 3 ◽  
Virus Core

scholarly journals Hepatitis C virus core protein, lipid droplets and steatosis

2007 ◽  
Vol 15 (3) ◽  
pp. 157-164 ◽  
Author(s):  
P. Roingeard ◽  
C. Hourioux
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Lipid Droplets ◽  
Core Protein ◽  
Virus Core

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

Pathogens ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 1327
Author(s):  
Abdellah Akil ◽  
Peixuan Song ◽  
Juan Peng ◽  
Claire Gondeau ◽  
Didier Samuel ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Lipid Droplet ◽  
Core Protein ◽  
Septin 9 ◽  
Host Cell Proteins ◽  
Filament Assembly ◽  
Microtubule Polymerization ◽  
Hcv Core Protein

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.

1140 HEPATITIS C VIRUS AND LIPID DROPLETS: ROLE OF ADIPOSE DIFFERENTIATION-RELATED PROTEIN IN LIPID DROPLET MORPHOLOGY AND VIRAL LIFE CYCLE

2013 ◽  
Vol 58 ◽  
pp. S464
Author(s):  
E. Branche ◽  
S. Clement ◽  
P. Levy ◽  
C. Parisot ◽  
S. Conzelmann ◽  
...  
Keyword(s):  
Life Cycle ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Lipid Droplet ◽  
Lipid Droplets ◽  
Viral Life Cycle ◽  
Related Protein ◽  
Adipose Differentiation ◽  
Droplet Morphology
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