Pathogenetic Mechanisms of Hepatitis C Virus-Induced B-Cell Lymphomagenesis

Hepatitis C virus (HCV) infection is probably the most common chronic viral infection and affects an estimated 180 million people worldwide, accounting for 3% of the global population. Although the liver is considered to be the primary target, extrahepatic manifestations are well recognized among pa...

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Main Authors: Fabio Forghieri, Mario Luppi, Patrizia Barozzi, Rossana Maffei, Leonardo Potenza, Franco Narni, Roberto Marasca
Format: Article
Language:English
Published: Wiley 2012-01-01
Series:Clinical and Developmental Immunology
Online Access:http://dx.doi.org/10.1155/2012/807351
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author Fabio Forghieri
Mario Luppi
Patrizia Barozzi
Rossana Maffei
Leonardo Potenza
Franco Narni
Roberto Marasca
author_facet Fabio Forghieri
Mario Luppi
Patrizia Barozzi
Rossana Maffei
Leonardo Potenza
Franco Narni
Roberto Marasca
author_sort Fabio Forghieri
collection DOAJ
description Hepatitis C virus (HCV) infection is probably the most common chronic viral infection and affects an estimated 180 million people worldwide, accounting for 3% of the global population. Although the liver is considered to be the primary target, extrahepatic manifestations are well recognized among patients with chronic HCV infection. Epidemiological studies have clearly demonstrated a correlation between chronic HCV infection and occurrence of B-cell non-Hodgkin's lymphomas (B-NHL). The clinical evidence that antiviral therapy has a significant role in the treatment at least of some HCV-associated lymphoproliferative disorders, especially indolent B-NHL, further supports the existence of an etiopathogenetic link. However, the mechanisms exploited by HCV to induce B-cell lymphoproliferation have so far not completely clarified. It is conceivable that different biological mechanisms, namely, chronic antigen stimulation, high-affinity interaction between HCV-E2 protein and its cellular receptors, direct HCV infection of B-cells, and “hit and run” transforming events, may be combined themselves and cooperate in a multifactorial model of HCV-associated lymphomagenesis.
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spelling doaj-art-5ca74bbbac13433586ab9cae15091d772025-08-20T02:04:59ZengWileyClinical and Developmental Immunology1740-25221740-25302012-01-01201210.1155/2012/807351807351Pathogenetic Mechanisms of Hepatitis C Virus-Induced B-Cell LymphomagenesisFabio Forghieri0Mario Luppi1Patrizia Barozzi2Rossana Maffei3Leonardo Potenza4Franco Narni5Roberto Marasca6Section of Hematology, Department of Oncology, Hematology, and Respiratory Diseases, University of Modena and Reggio Emilia, 41100 Modena, ItalySection of Hematology, Department of Oncology, Hematology, and Respiratory Diseases, University of Modena and Reggio Emilia, 41100 Modena, ItalySection of Hematology, Department of Oncology, Hematology, and Respiratory Diseases, University of Modena and Reggio Emilia, 41100 Modena, ItalySection of Hematology, Department of Oncology, Hematology, and Respiratory Diseases, University of Modena and Reggio Emilia, 41100 Modena, ItalySection of Hematology, Department of Oncology, Hematology, and Respiratory Diseases, University of Modena and Reggio Emilia, 41100 Modena, ItalySection of Hematology, Department of Oncology, Hematology, and Respiratory Diseases, University of Modena and Reggio Emilia, 41100 Modena, ItalySection of Hematology, Department of Oncology, Hematology, and Respiratory Diseases, University of Modena and Reggio Emilia, 41100 Modena, ItalyHepatitis C virus (HCV) infection is probably the most common chronic viral infection and affects an estimated 180 million people worldwide, accounting for 3% of the global population. Although the liver is considered to be the primary target, extrahepatic manifestations are well recognized among patients with chronic HCV infection. Epidemiological studies have clearly demonstrated a correlation between chronic HCV infection and occurrence of B-cell non-Hodgkin's lymphomas (B-NHL). The clinical evidence that antiviral therapy has a significant role in the treatment at least of some HCV-associated lymphoproliferative disorders, especially indolent B-NHL, further supports the existence of an etiopathogenetic link. However, the mechanisms exploited by HCV to induce B-cell lymphoproliferation have so far not completely clarified. It is conceivable that different biological mechanisms, namely, chronic antigen stimulation, high-affinity interaction between HCV-E2 protein and its cellular receptors, direct HCV infection of B-cells, and “hit and run” transforming events, may be combined themselves and cooperate in a multifactorial model of HCV-associated lymphomagenesis.http://dx.doi.org/10.1155/2012/807351
spellingShingle Fabio Forghieri
Mario Luppi
Patrizia Barozzi
Rossana Maffei
Leonardo Potenza
Franco Narni
Roberto Marasca
Pathogenetic Mechanisms of Hepatitis C Virus-Induced B-Cell Lymphomagenesis
Clinical and Developmental Immunology
title Pathogenetic Mechanisms of Hepatitis C Virus-Induced B-Cell Lymphomagenesis
title_full Pathogenetic Mechanisms of Hepatitis C Virus-Induced B-Cell Lymphomagenesis
title_fullStr Pathogenetic Mechanisms of Hepatitis C Virus-Induced B-Cell Lymphomagenesis
title_full_unstemmed Pathogenetic Mechanisms of Hepatitis C Virus-Induced B-Cell Lymphomagenesis
title_short Pathogenetic Mechanisms of Hepatitis C Virus-Induced B-Cell Lymphomagenesis
title_sort pathogenetic mechanisms of hepatitis c virus induced b cell lymphomagenesis
url http://dx.doi.org/10.1155/2012/807351
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