Background: Hepatitis C virus (HCV) infection is a well-documented etiological factor for hepatocellular carcinoma (HCC). As HCV shows remarkable genetic diversity, an interesting and important issue is whether such a high viral genetic diversity plays a role in the incidence of HCC. Prior data on this subject are conflicting.
Objectives: Potential association between HCV genetic mutations or strain variability and HCC incidence has been examined through a comparative genetic analysis merely focused on a single HCV subtype (genotype 4a) in a single country (Egypt).
Study Design: The study focused on three HCV sequence datasets with explicit sampling dates and disease patterns. An overlapping HCV Core/E1 domain from three datasets was used as the target for comparative analysis through genetic and phylogenetic approaches.
Results: Based on partial Core/E1 domain (387 bp), genetic and phylogenetic analysis did not identify any HCC-specific viral mutations and strains, respectively.
Conclusions: The Core/E1 domain of HCV genotype 4a in Egypt does not contain HCC-specific mutations or strains. Additionally, sequence errors resulting from the polymerase chain reaction, together with a strong evolutionary pressure on HCV in patients with end-stage liver disease, have significant potential to bias data generation and interpretation.
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http://dx.doi.org/10.1016/j.jcv.2011.08.022 | DOI Listing |
Arch Virol
June 2012
Department of Infectious Diseases, Hepatology Unit, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Evidence has shown that the p7, NS2 and NS3 genes affect the outcome of pegylated-IFN-α/ribavirin (PEG-IFN/RBV) combination therapy in different populations with HCV infections. Here, we test the hypothesis that diversity in the p7, NS2 and NS3 genes influences the probability of obtaining either a sustained (SVR) or non-sustained (non-SVR) viral response in Chinese patients with genotype 1b chronic hepatitis C. There were significantly more unique variations in the p7, NS2 and NS3 genes in the sequences from SVR than non-SVR patients.
View Article and Find Full Text PDFJ Clin Virol
December 2011
Division of Gastroenterology and Hepatology, Department of Internal Medicine, Saint Louis University School of Medicine, St. Louis, MO 63104, USA.
Background: Hepatitis C virus (HCV) infection is a well-documented etiological factor for hepatocellular carcinoma (HCC). As HCV shows remarkable genetic diversity, an interesting and important issue is whether such a high viral genetic diversity plays a role in the incidence of HCC. Prior data on this subject are conflicting.
View Article and Find Full Text PDFVirology
May 1999
Medical Research Council Virology Unit, Church Street, Glasgow, G11 5JR, United Kingdom.
Several studies have implicated hepatitis C virus (HCV) core in influencing the expression of host genes. To identify cellular factors with a possible role in HCV replication and pathogenesis, we looked for cellular proteins that interact with the viral core protein. A human liver cDNA library was screened in a yeast two-hybrid assay to identify cellular proteins that bind to core.
View Article and Find Full Text PDFJ Hepatol
December 1996
Institute for Virology Johannes-Gutenberg-University of Main, Germany.
Hepatitis C virus (HCV) is the major etiological agent of posttransfusion and community-acquired non-A, non-B hepatitis. It is an enveloped virus, grouped as a separate genus in the Flaviviridae family. The plus-stranded RNA genome encodes a polyprotein of about 3000 amino acids with the structural proteins core, E1 and E2 residing in the amino terminal quarter of the polyprotein and the nonstructural proteins NS2, NS3, NS4A, NS4B, NS5A and NS5B in the remainder.
View Article and Find Full Text PDFJ Hepatol
June 1994
Consorzio per le Biotecnologie, Consiglio Nazionale delle Ricerche (CNR), School of Medicine, University of Brescia, Italy.
The putative hepatitis C virus core protein has a predicted molecular weight of about 22 kD and contains two carboxy (COOH)-terminal hydrophobic domains. The cleavages generating the hepatitis C virus structural proteins (core, E1 and E2) are catalyzed by host signal peptidases. In the present study, we investigated the processing and intracellular localization of the hepatitis C virus core protein expressed in mammalian cells.
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