scholarly journals Chronic Hepatitis C Virus Infection Breaks Tolerance and Drives Polyclonal Expansion of Autoreactive B Cells

2012 ◽  
Vol 19 (7) ◽  
pp. 1027-1037 ◽  
Author(s):  
Jill E. Roughan ◽  
Kathryn M. Reardon ◽  
Kristin E. Cogburn ◽  
Heribert Quendler ◽  
Paul J. Pockros ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
B Cells ◽  
B Cell ◽  
Chronic Hepatitis C ◽  
Cell Subset ◽  
Autoreactive B Cells ◽  
Chronic Hepatitis C Virus ◽  
Chronic Hcv

ABSTRACTChronic Hepatitis C virus (HCV) infection has been linked with B cell lymphoproliferative disorders and several autoimmune-related diseases. The mechanisms of how chronic viral infection affects B cell development and predisposes the patients to autoimmune manifestations are poorly understood. In this study, we established an experimental system to probe the B cell responses and characterize the antibodies from chronic-HCV-infected individuals. We identified an unusual polyclonal expansion of the IgM memory B cell subset in some patients. This B cell subset is known to be tightly regulated, and autoreactive cells are eliminated by tolerance mechanisms. Genetic analysis of the immunoglobulin (Ig) heavy chain variable gene (VH) sequences of the expanded cell population showed that the levels of somatic hypermutation (SHM) correlate with the extent of cell expansion in the patients and that the VHgenes exhibit signs of antigen-mediated selection. Functional analysis of the cloned B cell receptors demonstrated autoreactivity in some of the expanded IgM memory B cells in the patients which is not found in healthy donors. In summary, this study demonstrated that, in some patients, chronic HCV infection disrupts the tolerance mechanism that normally deletes autoreactive B cells, therefore increasing the risk of developing autoimmune antibodies. Long-term follow-up of this expanded B cell subset within the infected individuals will help determine whether these cells are predictors of more-serious clinical manifestations.

Circulating and inducible IL-32α in chronic hepatitis C virus infection

2019 ◽  
Vol 2 (1) ◽  
pp. 23-30
Author(s):  
Mark Collister ◽  
Julia Rempel ◽  
Jiaqi Yang ◽  
Kelly Kaita ◽  
Zach Raizman ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Chronic Hepatitis C ◽  
Mononuclear Cells ◽  
Peripheral Blood Mononuclear ◽  
Chronic Hepatitis C Virus ◽  
Chronic Hcv

Background: Interleukin 32 (IL-32) is a recently described pro-inflammatory cytokine implicated in chronic hepatitis C virus (HCV)-related inflammation and fibrosis. IL-32α is the most abundant IL-32 isoform. Methods: Circulating IL-32α levels were documented in patients with chronic HCV infections ( n = 31) and compared with individuals who spontaneously resolved HCV infection ( n = 14) and HCV-naive controls ( n = 20). In addition, peripheral blood mononuclear cells (PBMC) from the chronic HCV ( n = 12) and HCV-naive ( n = 9) cohorts were investigated for responses to HCV core and non-structural (NS)3 protein induced IL-32α production. Finally, correlations between IL-32α levels, hepatic fibrosis and subsequent responses to interferon-based therapy were documented in patients with chronic HCV. Results: Circulating IL-32α levels in patients with chronic HCV were similar to those of spontaneously resolved and HCV-naive controls. HCV protein induced IL-32α responses were similar in chronic HCV patients and HCV-naive controls. In patients with chronic HCV, serum IL-32α levels correlated with worsening METAVIR fibrosis (F) scores from F0 to F3 ( r = 0.596, P < 0.001) as did NS3 induced IL-32α responses ( r = 0.837, P < 0.05). However, these correlations were not sustained with the inclusion of IL-32α levels at F4 scores, suggesting events at F4 interfere with IL-32α synthesis or release. In chronic HCV patients who underwent treatment ( n = 28), baseline in vivo and in vitro induced IL-32α concentrations were not predictive of therapeutic outcomes. Conclusions: IL-32α activity is associated with worsening fibrosis scores in non-cirrhotic, chronic HCV patients.

scholarly journals Patients With Chronic Hepatitis C Virus Infection Are at an Increased Risk of Colorectal Cancer: A Nationwide Population-Based Case-Control Study in Taiwan

2021 ◽  
Vol 10 ◽  
Author(s):  
Fu-Hsiung Su ◽  
Chyi-Huey Bai ◽  
Thi Nga Le ◽  
Chih-Hsin Muo ◽  
Shih-Ni Chang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Chronic Hepatitis ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Chronic Hepatitis C ◽  
Case Control Study ◽  
Case Control ◽  
Chronic Hepatitis C Virus ◽  
Chronic Hcv ◽  
Control Study

AimStudies evaluating colorectal cancer (CRC) risk associated with chronic hepatitis C virus (HCV) infection are limited.MethodsIn this case-control study, we identify 67,670 CRC cases newly diagnosed from 2005 to 2011 and randomly selected 67,670 controls without HCV and CRC from the same database, frequency matched by age and sex of cases.ResultsResults of logistic regression analysis revealed that the adjusted odds ratio (aOR) of CRC was 1.16 (95% confidence interval [CI] = 1.08–1.24, p &lt; 0.001) in association with chronic HCV. The CRC risk was slightly greater for women than for men. The risk decreased with age, with the aOR decreased from 2.26 (95% CI = 1.32–3.87, p = 0.003) in patients under 45 years old to 1.31 (95% CI = 1.10–1.55, p = 0.03) in patients aged 50–59, and 1.10 (95% CI = 1.00–1.22, p = 0.061) in patients aged over 70.ConclusionsOur findings suggested that patients with chronic HCV infection are at an elevated risk of developing CRC. Our data also imply that the CRC prevention programs are needed to target younger HCV patients.

scholarly journals Antiviral Treatment Down-Regulates Peripheral B-Cell CD81 Expression and CD5 Expansion in Chronic Hepatitis C Virus Infection

2004 ◽  
Vol 78 (10) ◽  
pp. 5533-5533
Author(s):  
Eli Zuckerman ◽  
Aharon Kessel ◽  
Gleb Slobodin ◽  
Edmond Sabo ◽  
Daniel Yeshurun ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Virus Infection ◽  
B Cell ◽  
Chronic Hepatitis C ◽  
Antiviral Treatment ◽  
Hepatitis C Virus Infection ◽  
Chronic Hepatitis C Virus

The effect of anti-viral treatment on peripheral B-cell CD81 expression and CD5 expansion in chronic hepatitis C virus (HCV) infection

2002 ◽  
Vol 36 ◽  
pp. 95
Author(s):  
Eli Zuckerman ◽  
Aharon Kessel ◽  
Gleb Slobodin ◽  
Edmond Sabo ◽  
Daniel Yeshurun ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
B Cell ◽  
Chronic Hepatitis C ◽  
Hcv Infection ◽  
Chronic Hepatitis C Virus

The 1F7 idiotype is selectively expressed on CD5 + B cells and elevated in chronic hepatitis C virus infection

2009 ◽  
Vol 87 (6) ◽  
pp. 457-463 ◽  
Author(s):  
Tigran K Davtyan ◽  
Marine P Hovsepyan ◽  
Levon M Mkhitaryan ◽  
Gagik S Hakobyan ◽  
Aiden Brazil ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
B Cells ◽  
Virus Infection ◽  
Chronic Hepatitis C ◽  
Hepatitis C Virus Infection ◽  
Chronic Hepatitis C Virus

scholarly journals Atherosclerosis as a Possible Extrahepatic Manifestation of Chronic Hepatitis C Virus Infection

2014 ◽  
Vol 8s3 ◽  
pp. CMC.S17069 ◽  
Author(s):  
Nobukazu Ishizaka ◽  
Yuko Ishizaka ◽  
Minoru Yamkado
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Chronic Hepatitis C ◽  
Target Population ◽  
Hcv Infection ◽  
Inverse Association ◽  
Vascular Changes ◽  
Chronic Hepatitis C Virus ◽  
Chronic Hcv

Chronic infection and associated inflammation may play a role in various unfavorable pathologic conditions, including atherosclerosis. Chronic hepatitis C virus (HCV) infection is thought to be associated with a higher prevalence of atherosclerotic vascular changes in the coronary artery, cerebrovascular artery, and carotid artery; however, little is known about the precise mechanisms by which HCV enhances atherogenic processes. Furthermore, some studies have found no association, or even an inverse association, between HCV infection and atherosclerotic vascular changes or cardiovascular events. Differences in data regarding the mode of association may be because of variations in sample size, target population, and study design. Nevertheless, physicians should be aware of cardiovascular disorders as a possible comorbidity – owing to their considerable consequences – among patients with chronic HCV infection.

scholarly journals Enhanced Activation of Memory, but Not Naïve, B Cells in Chronic Hepatitis C Virus-Infected Patients with Cryoglobulinemia and Advanced Liver Fibrosis

PLoS ONE ◽  
2013 ◽  
Vol 8 (6) ◽  
pp. e68308 ◽  
Author(s):  
Deanna M. Santer ◽  
Mang M. Ma ◽  
Darren Hockman ◽  
Abdolamir Landi ◽  
D. Lorne J. Tyrrell ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
B Cells ◽  
Liver Fibrosis ◽  
Chronic Hepatitis C ◽  
Chronic Hepatitis C Virus ◽  
Advanced Liver Fibrosis

scholarly journals Treatment options for chronic hepatitis C virus infection

2006 ◽  
Vol 59 (11-12) ◽  
pp. 560-566
Author(s):  
Ivanko Bojic ◽  
Ljubisa Dokic ◽  
Svetlana Minic
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Chronic Hepatitis C ◽  
Induction Therapy ◽  
Hcv Infection ◽  
Initiation Factor ◽  
Chronic Hepatitis C Virus ◽  
Chronic Hcv Infection ◽  
Chronic Hcv

Introduction. The incidence of chronic hepatitis C virus (HCV) infection is rather high. Its most frequent consequences are chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. Treatment of chronic HCV infection. In treatment of chronic HCV infection, interferons have antiviral, anriproliferative, and immunoregulatory action. Within the cell, they induce protein synthesis, inhibiting viral replication. The most important among them are RNA dependent protein kinase, and eukaryotic initiation factor. However, viral proteins prevent their phosphorylation and activation. In order to overcome this problem, treatment is prolonged, higher doses of IFN are used, as well as induction therapy. The optimal period for viral response is 52 weeks, while induction therapy has shown controversial results. .

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