Hepatitis C virus F protein inhibits cell apoptosis by activation of intracellular NF‐κB pathway

Shao, Shengwen; Wu, Wen‐Bin; Bian, Zhong-qi; Yu, Jianguo; Zhao, Ping; Zhao, Lan‐Juan; Zhu, Shiying; Qi, Zhongtian

doi:10.1111/j.1872-034x.2008.00452.x

Cited by 17 publications

(14 citation statements)

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“…It has been reported that HCV F protein inhibits the apoptosis of HepG2 cells, a human liver carcinoma cell line, by activation of NF-B activity [42]. Taken together with these study findings, NF-B activity may be finely modulated to facilitate HCV replication (inhibited apoptosis in target liver cells by activation of NF-B activity) and to evade immune response (increased apoptosis of immune cells by inhibition of NF-B activity).…”

Section: Discussionsupporting

confidence: 65%

Functional changes, increased apoptosis, and diminished nuclear factor–κB activity of myeloid dendritic cells during chronic hepatitis C infection

2010

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Section: Discussionsupporting

confidence: 65%

Functional changes, increased apoptosis, and diminished nuclear factor–κB activity of myeloid dendritic cells during chronic hepatitis C infection

2010

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“…In fact, recent studies indicated that ARFP is an unstable protein that associates with the endoplasmic reticulum [13] and may play a role in the regulation of gene expression, cell signaling and apoptosis [14][15][16][17], as well as in altering immune responses [18]. These potential properties of the ARFP have attracted recently much attention and intensified the studies of its features.…”

mentioning

confidence: 96%

Expression and characterization of Escherichia coli derived hepatitis C virus ARFP/F protein

et al. 2012

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Genome of the hepatitis C virus (HCV) contains a long open reading frame encoding a polypro tein that is cleaved into 10 proteins. Recently, a novel, so called "ARFP/F", or "core+1," protein, which is expressed through a ribosomal frame shift within the capsid coding sequence, has been described. Herein, to produce and characterize a recombinant form of this protein, the DNA sequence corresponding to the ARFP/F protein (amino acid 11-161) was amplified using a frame shifted forward primer exploiting the capsid sequence of the lb subtype as a template. The amplicon was cloned into the pET 24a vector and expressed in different Escherichia coli strains. The expressed protein (mostly as insoluble inclusion bodies) was purified under denaturing conditions on a nickel nitrilotriacetic acid (Ni NTA) affinity column in a sin gle step with a yield of 5 mg/L of culture media. After refolding steps, characterization of expressed ARFP/F was performed by SDS PAGE and Western blot assay using specific antibodies. Antigenic properties of the protein were verified by ELISA using HCV infected human sera and by its ability for a strong and specific interaction with sera of mice immunized with the peptide encoding a dominant ARFP/F B cell epitope. The antigenicity plot revealed 3 major antigenic domains in the first half of the ARFP/F sequence. Immunization of BALB/c mice with the ARFP/F protein elicited high titers of IgG indicating the relevance of produced protein for induction of a humoral response. In conclusion, possibility of ARFP/F expression with a high yield and immunogenic potency of this protein in a mouse model have been demonstrated.

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“…In addition, alternative translation products (F protein) have been detected from a reading frame overlapping the core gene (core + 1/ARFP) [16,17] . Possible roles in regulation of gene expression, cell signalling and apoptosis have been suggested [18][19][20] . Short untranslated regions at each end of the genome (5'-NCR and 3'-NCR) are required for its translation and replication [21,22] .…”

Section: Introductionmentioning

confidence: 99%

Hepatitis C virus genetic variability and evolution

Echeverría

Moratorio

Cristina

et al. 2015

WJH

100

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Hepatitis C virus (HCV) has infected over 170 million people worldwide and creates a huge disease burden due to chronic, progressive liver disease. HCV is a singlestranded, positive sense, RNA virus, member of the Flaviviridae family. The high error rate of RNA-dependent RNA polymerase and the pressure exerted by the host immune system, has driven the evolution of HCV into 7 different genotypes and more than 67 subtypes. HCV evolves by means of different mechanisms of genetic variation. On the one hand, its high mutation rates generate the production of a large number of different but closely related viral variants during infection, usually referred to as a quasispecies. The great quasispecies variability of HCV has also therapeutic implications since the continuous generation and selection of resistant or fitter variants within the quasispecies spectrum might allow viruses to escape control by antiviral drugs. On the other hand HCV exploits recombination to ensure its survival. This enormous viral diversity together with some host factors has made it difficult to control viral dispersal. Current treatment options involve pegylated interferon-α and ribavirin as dual therapy or in combination with a direct-acting antiviral drug, depending on the country. Despite all the efforts put into antiviral therapy studies, eradication of the virus or the development of a preventive vaccine has been unsuccessful so far. This review focuses on current available data reported to date on the genetic mechanisms driving the molecular evolution of HCV populations and its relation with the antiviral therapies designed to control HCV infection. Hepatitis C virus genetic variability and evolution no preventive vaccine, and though antiviral therapy has been improved in the past few years, not all patients eradicate the virus as a result of it. The main reason lies in the intrinsic genetic variability that characterises RNA viruses, such as HCV, whose RNA polymerase lacks proof-reading activity, leading to a high mutation rate and the generation of a wide range of genome variants better known as a quasispecies. Therefore this review summarises current data on HCV quasispecies dynamics, antiviral therapy and recombination events.Echeverría N, Moratorio G, Cristina J, Moreno P. Hepatitis C virus genetic variability and evolution. World J Hepatol 2015; 7(6): 831845 Available from:

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Hepatitis C virus F protein inhibits cell apoptosis by activation of intracellular NF‐κB pathway

Abstract: HCV F protein can over-activate NF-kappaB signal pathway, which makes HepG2-F cells able to resist TNF-alpha induced apoptosis.

Cited by 17 publications

References 32 publications

Functional changes, increased apoptosis, and diminished nuclear factor–κB activity of myeloid dendritic cells during chronic hepatitis C infection

Functional changes, increased apoptosis, and diminished nuclear factor–κB activity of myeloid dendritic cells during chronic hepatitis C infection

Expression and characterization of Escherichia coli derived hepatitis C virus ARFP/F protein

Hepatitis C virus genetic variability and evolution

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