Peripheral B Cells as Reservoirs for Persistent HCV Infection

Masahiko Ito,Hideki Kusunoki,Toshiaki Mizuochi

doi:10.3389/fmicb.2011.00177

Abstract

Peripheral B Cells as Reservoirs for Persistent HCV Infection

Highlights

The liver is considered the primary and main target of Hepatitis C virus (HCV) infection, extrahepatic manifestations such as mixed cryoglobulinemia, a systemic immune complex-mediated disorder characterized by B cell proliferation that may evolve into overt B cell non-Hodgkin’s lymphoma (B-NHL), are often recognized among patients persistently infected with HCV (Agnello et al, 1992; Zuckerman et al, 1997)
In order to determine how HCV evades antiviral innate immune responses that are normally induced in B cells, we analyzed expression levels of IFN-β in peripheral B cells of chronic hepatitis C (CHC) patients because type I IFN plays a critical role in the antiviral innate immune response
We found that HCV infection failed to trigger antiviral immune responses, such as IFN-β production, in B cells of CHC patients (Ito et al, 2010b)

Summary

Introduction

The liver is considered the primary and main target of HCV infection, extrahepatic manifestations such as mixed cryoglobulinemia, a systemic immune complex-mediated disorder characterized by B cell proliferation that may evolve into overt B cell non-Hodgkin’s lymphoma (B-NHL), are often recognized among patients persistently infected with HCV (Agnello et al, 1992; Zuckerman et al, 1997). In accordance with this notion, our recent study clearly demonstrated that HCV infects and may replicate in the peripheral CD19+ B cells of chronic hepatitis C (CHC) patients (Ito et al, 2010a). In order to determine how HCV evades antiviral innate immune responses that are normally induced in B cells, we analyzed expression levels of IFN-β in peripheral B cells of CHC patients because type I IFN plays a critical role in the antiviral innate immune response.

Results

Conclusion