scholarly journals HCV Infection and B-Cell Lymphomagenesis

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Masahiko Ito ◽  
Hideki Kusunoki ◽  
Keiko Mochida ◽  
Kazunari Yamaguchi ◽  
Toshiaki Mizuochi
Keyword(s):  
B Cells ◽  
B Cell ◽  
Chronic Infection ◽  
Recent Literature ◽  
Epidemiological Data ◽  
Mixed Cryoglobulinemia ◽  
Hcv Infection ◽  
Chronic Hcv Infection ◽  
Chronic Hcv

Hepatitis C virus (HCV) has been recognized as a major cause of chronic liver diseases worldwide. It has been suggested that HCV infects not only hepatocytes but also mononuclear lymphocytes including B cells that express the CD81 molecule, a putative HCV receptor. HCV infection of B cells is the likely cause of B-cell dysregulation disorders such as mixed cryoglobulinemia, rheumatoid factor production, and B-cell lymphoproliferative disorders that may evolve into non-Hodgkin's lymphoma (NHL). Epidemiological data indicate an association between HCV chronic infection and the occurrence of B-cell NHL, suggesting that chronic HCV infection is associated at least in part with B-cell lymphomagenesis. In this paper, we aim to provide an overview of recent literature, including our own, to elucidate a possible role of HCV chronic infection in B-cell lymphomagenesis.

708 THE ROLE OF REGULATORY B-CELLS IN CHRONIC HCV INFECTION AND THEIR RELATION TO HCV-ASSOCIATED AUTOIMMUNITY

2010 ◽  
Vol 52 ◽  
pp. S275
Author(s):  
E. Zuckerman ◽  
C. Dashkovsky ◽  
R. Peri ◽  
E. Sabo ◽  
E. Toubi
Keyword(s):  
B Cells ◽  
Hcv Infection ◽  
Regulatory B Cells ◽  
Chronic Hcv Infection ◽  
Chronic Hcv

scholarly journals Genetic Variants in JAK1 Gene and Susceptibility to Hepatitis C Viral Infection in Iraq

2016 ◽  
Vol 10 (1) ◽  
pp. 37-41
Author(s):  
Fatima Abood Chaloob
Keyword(s):  
Hepatitis C ◽  
Hcv Infection ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Global Challenge ◽  
Pcr Products ◽  
Chronic Hcv Infection ◽  
Chronic Hcv ◽  
Apparently Healthy

Infection with hepatitis C virus (HCV) imposes a global challenge with over 180 million cases worldwide. Only few patients spontaneously had their virus neutralized, while most patients develop chronic HCV infection. This implies a key role of genetic factors in viral clearance or persistence. The current study aimed at clarifying the effect of certain single nucleotide polymorphisms (SNPs) on individual's susceptibility to HCV infection.  A total of 60 patients with confirmed HCV infection and 35 apparently healthy individuals were enrolled in this study. Blood sample was obtained from each participant, from which DNA was extracted. The JAK1gene was amplified with conventional PCR technique using three sets of primers targeting three SNPs in this gene: rs2780895, rs4244165 and rs17127024. Restriction fragment length polymorphism (RFLP) was used for genotyping of PCR products. Each of rs2780895 and rs17127024 had two genotypes in both patients and controls, however, only the heterozygous genotype of the SNP rs2780895 (CT) significantly associated with the susceptibility to HCV. The SNP rs4244165 appeared in only with homozygous wild genotype (GG) in both patients and controls. It can be concluded that allele T of the SNP rs2780895 could be considered as a risk factor for infection with HCV

scholarly journals Increased killer B cells in chronic HCV infection may lead to autoimmunity and increased viral load

2018 ◽  
Vol 193 (2) ◽  
pp. 183-193 ◽  
Author(s):  
N. Eiza ◽  
E. Zuckerman ◽  
M. Carlebach ◽  
T. Rainis ◽  
Y. Goldberg ◽  
...  
Keyword(s):  
Viral Load ◽  
B Cells ◽  
Hcv Infection ◽  
Chronic Hcv Infection ◽  
Chronic Hcv

Lack of Hcv Infection in Malignant, Cells Refutes the Hypothesis of a Direct Transforming Action of the Virus in the Pathogenesis of Hcv-Associated B-Cell Nhls

2002 ◽  
Vol 88 (5) ◽  
pp. 400-406 ◽  
Author(s):  
Salvatore De Vita ◽  
Valli De Re ◽  
Domenico Sansonno ◽  
Annunziata Gloghini ◽  
Daniela Gasparotto ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Hcv Infection ◽  
Low Grade ◽  
Immunoglobulin Gene ◽  
Pathogenetic Role ◽  
Exogenous Trigger ◽  
Grade One ◽  
Hodgkin's Lymphomas

Aims and background Preliminary evidence suggests that hepatitis C virus (HCV) might play a pathogenetic role in autoimmune-related, non-malignant B-cell lymphoproliferation, as well as in a subset of B-cell non-Hodgkin's lymphomas (NHLs). With regard to the mechanism(s) by which HCV might favor B-cell expansion and malignant transformation, most data support an indirect pathogenetic role of the virus as an exogenous trigger. A direct oncogenetic role of HCV by direct cell infection and deregulation has only been hypothesized on the basis of the lymphotropism of the virus. Methods In this study we investigated the possible HCV infection of NHL B cells by means of sensitive and quantitative polymerase chain reaction (PCR) on affinity-purified neoplastic cells, and by HCV-specific immunohistochemistry and in situ hybridization. Results HCV infection of neoplastic B cells was documented in only three cases, namely the low-grade B-cell NHLs that arose in the course of mixed cryoglobulinemia syndrome (MC). HCV infection, below one viral genome per cell, was detectable only by PCR. All the remaining low-grade (one case) and high-grade B-cell NHLs (two cases) were HCV uninfected. Previous immunoglobulin gene analyses were consistent with an antigen-driven B-cell lymphoproliferation in the studied cases. Conclusions Overall, our data are consistent with an indirect oncogenetic role of HCV in B-cell lymphomagenesis as an exogenous trigger. Infection of B cells by HCV appears possible in some NHL subsets, but the implications remain unknown.

scholarly journals HCV-associated mixed cryoglobulinemia and b-cell non-Hodgkin's lymphoma - pathogenetically related problems

2018 ◽  
Vol 90 (6) ◽  
pp. 112-120 ◽  
Author(s):  
S Yu Milovanova ◽  
L V Lysenko (Kozlovskaya) ◽  
L Yu Milovanova ◽  
N N Mrykhin ◽  
A V Russkih ◽  
...  
Keyword(s):  
B Cell ◽  
Antiviral Therapy ◽  
Hodgkin’S Lymphoma ◽  
Meta Analysis ◽  
Epidemiological Data ◽  
Mixed Cryoglobulinemia ◽  
Hodgkin's Lymphoma ◽  
Non Hodgkin’S Lymphoma ◽  
Non Hodgkin's Lymphoma

Hepatitis C virus (HCV) is a global population problem due to its high prevalence, usually late diagnosis, the difficulties of treatment. In the prognosis of patients with HCV not only hepatic, but increasingly frequent of extrahepatic HCV manifestations, such as mixed cryoglobulinemia (CG), are important. Mixed CG is currently considered as a B-cell benign lymphoproliferative disorders. The role of HCV virus in the pathogenesis of lymphoproliferative diseases is confirmed by a large number of epidemiological studies, as well as by the effectiveness of antiviral therapy in patients with non-Hodgkin’s lymphoma (NHL). The purpose of the review was to provide an overview of recent literature data and the meta-analysis of epidemiological data explaining the role of HCV in the development of NHL. The review also discusses the treatment for HCV-associated NHL by antiviral therapy or other therapeutic options, such as chemotherapy.

Impaired insulin exocytosis in chronic hepatitis C infection: contributory role of p38δ MAPK–protein kinase D–golgi complex axis

2020 ◽  
Vol 134 (12) ◽  
pp. 1449-1456
Author(s):  
Parimala Narne
Keyword(s):  
Hepatitis C ◽  
Protein Kinase ◽  
Golgi Complex ◽  
Hcv Infection ◽  
Protein Kinase D ◽  
Cell Dysfunction ◽  
Chronic Hcv Infection ◽  
Chronic Hcv ◽  
Insulin Exocytosis

Abstract Hepatitis C virus (HCV) infection and chronic hepatitis C (CHC) are associated with a measurable risk of insulin resistance (IR)/impaired glucose tolerance (IGT)/diabetes mellitus (DM). While loss of hepatic endocrine function contributes to liver cirrhosis in diabetic patients, onset and progression of IR/IGT to diabetes and exacerbation of incident hyperglycemia are ostensibly linked with chronic HCV infection. In this regard, the study by Chen J et al. appearing in Clinical Science (2020) (134(5) https://doi.org/10.1042/CS20190900) attempts to understand the mechanisms underlying the savaging effects of chronic HCV infection on insulin-producing pancreatic β-cells and hence diabetic onset. The study investigated the role of mitogen-activated protein kinase (MAPK) p38δ–protein kinase D (PKD)–golgi complex axis in impacting insulin exocytosis. It was inferred that an insulin secretory defect of pancreatic β-cells, owing to disrupted insulin exocytosis, to an extent explains β-cell dysfunction in HCV-infected or CHC milieu. HCV infection negatively regulates first-phase and second-phase insulin secretion by impinging on PKD-dependent insulin secretory granule fission at trans-golgi network and insulin secretory vesicle membrane fusion events. This commentary highlights the study in question, that deciphered the contribution of p38δ MAPK–PKD–golgi complex axis to β-cell dysfunction in CHC milieu. This pivotal axis proffers a formidable therapeutic opportunity for alleviation of double burden of glucose abnormalities/DM and CHC.

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