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 ◽  
...  
2000 ◽  
Vol 74 (4) ◽  
pp. 1736-1741 ◽  
Author(s):  
Hiroshi Aoki ◽  
Junpei Hayashi ◽  
Mitsuhiko Moriyama ◽  
Yasuyuki Arakawa ◽  
Okio Hino

ABSTRACT Persistent hepatitis C virus (HCV) infection is a major cause of chronic liver dysfunction in humans and is epidemiologically closely associated with the development of human hepatocellular carcinoma. Among HCV components, core protein has been reported to be implicated in cell growth regulation both in vitro and in vivo, although mechanisms explaining those effects are still unclear. In the present study, we identified that members of the 14-3-3 protein family associate with HCV core protein. 14-3-3 protein bound to HCV core protein in a phosphoserine-dependent manner. Introduction of HCV core protein caused a substantial increase in Raf-1 kinase activity in HepG2 cells and in a yeast genetic assay. Furthermore, the HCV core–14-3-3 interaction was essential for Raf-1 kinase activation by HCV core protein. These results suggest that HCV core protein may represent a novel type of Raf-1 kinase-activating protein through its interaction with 14-3-3 protein and may contribute to hepatocyte growth regulation.


2005 ◽  
Vol 334 (3) ◽  
pp. 901-906 ◽  
Author(s):  
Nelson Acosta-Rivero ◽  
Armando Rodriguez ◽  
Alexis Mussachio ◽  
Johana Poutu ◽  
Viviana Falcon ◽  
...  

2007 ◽  
Vol 366 (1) ◽  
pp. 37-45 ◽  
Author(s):  
Rémi Fromentin ◽  
Nathalie Majeau ◽  
Marie-Eve Laliberté Gagné ◽  
Annie Boivin ◽  
Jean-Baptiste Duvignaud ◽  
...  

2010 ◽  
Vol 30 (9) ◽  
pp. 1324-1331 ◽  
Author(s):  
Fusao Ikeda ◽  
Hiromichi Dansako ◽  
Go Nishimura ◽  
Kyoko Mori ◽  
Yoshinari Kawai ◽  
...  

2006 ◽  
Vol 44 ◽  
pp. S168
Author(s):  
M. Zimmermann ◽  
C. Flechsig ◽  
K. Haugg ◽  
G. Adler ◽  
N. Dikopoulos

2008 ◽  
Vol 89 (8) ◽  
pp. 1890-1900 ◽  
Author(s):  
Wing Chia-Ming Chuang ◽  
Jean-Pierre Allain

To date, all studies regarding hepatitis C virus (HCV) F protein have been based on expression in vitro/in vivo of recombinant protein or monoclonal antibodies derived from genotype 1a or 1b sequences, but not from other genotypes. The objective of this study was to prepare a putative genotype 2 recombinant F protein and evaluate its reactivity in plasma from individuals with chronic HCV infection or who had recovered from infection. One genotype 2 strain was selected for F protein (F-2) and core expression in bacterial culture. An ELISA was developed and applied to samples from patients with chronic infection or recovered infection of various genotypes. The anti-F-2 response in 117 samples showed a significantly higher reactivity in chronic than in recovered HCV-infected blood donors (P<0.001), but no difference was found among genotypes. However, the correlation between anti-F and anti-core was more significant in genotypes 1 and 2 than in genotype 3. Anti-F-2 titres were also significantly higher in chronic than in recovered individuals (P<0.0001). Antibody titres to recombinant genotype 2 core protein or to genotype 1 multiple proteins used in commercial anti-HCV assays paralleled the anti-F-2 end-point antibody titre. This study thus demonstrated the antigenicity of genotype 2 HCV F protein, although the exact location of the natural frameshift position remains unknown. The difference in anti-F-2 response between chronic and recovered infection, the cross-reactivity irrespective of genotype and the correlation of antibody response with structural and non-structural antigens suggest that the immune response to F protein is an integral part of the natural HCV infection.


2012 ◽  
Vol 56 ◽  
pp. S342
Author(s):  
S.J. Li ◽  
F. Chen ◽  
S.P. Li ◽  
M. Zheng ◽  
X. Xing ◽  
...  

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