Expansion of innate CD5pos B cells expressing high levels of CD81 in hepatitis C virus infected liver

Curry, Michael P.; Golden-Mason, Lucy; Doherty, Derek G.; Deignan, Tina; Norris, Suzanne; Duffy, Margaret; Nolan, Niamh; Hall, William W.; Hegarty, John E.; O’Farrelly, Cliona

doi:10.1016/s0168-8278(03)00075-8

Cited by 70 publications

(36 citation statements)

References 48 publications

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“…Our data, 36 combined with those from the literature, [37][38][39] indicate a significant expansion of CD5 ϩ B cells in the peripheral blood of these patients. It can be speculated that the increased frequency of t(14;18) in blood leukocytes of either cryoglobulinemic or non-cryoglobulinemic HCV-infected patients does not reflect a true increase of its incidence, but may be a confounding factor related to the increased proportion of circulating B cells in these patients.…”

Section: Discussionsupporting

confidence: 81%

HCV-Associated B Cell Clonalities in the Liver Do Not Carry the t(14;18) Chromosomal Translocation *

Sansonno

Tucci

et al. 2005

Hepatology

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H epatitis C virus (HCV), a positive-strand enveloped RNA virus belonging to the Flaviviridae family, genus Hepacivirus, causes acute and chronic liver damage. 1 The mechanisms responsible for the tissue injury are poorly understood. 2 HCV often leads to hepatocellular carcinoma and, less frequently, to B-cell non-Hodgkin lymphoma (B-NHL). [3][4][5] HCV is mainly characterized by the failure to generate an effective immune response. Derangement of the B cell immune response has recently been explored by analyses of the size and sequence of complementarity determining region-3 (CDR-3) in the variable diversity joining (VDJ) segment of immunoglobulin heavy chain (IgH), which provide a molecular footprint of the overall B cell receptor (BCR) repertoire. 6 CDR H 3 is the segment of the Ig molecules that most closely interacts with the foreign immunogenic peptides and triggers the adaptive B cell immune response. BCRs of different specificities are generated by different combinations of V, D, and J gene segments to maximize CDR H 3 diversity and to provide the unique specificity of BCR. 7 Because of the lack of an efficient cell culture system for HCV, functions of most virus-encoded proteins have been established by analogy to other viruses and by homology to known proteins. HCV core protein modulates gene transcription, cell proliferation, and cell death. 8 NS3-encoded protein shows numerous interactions with cellular components, including protein-kinases, p53, and histones. 9 NS5A protein has been found to contain a Bcl-2 (B-cell lymphoma-2) homology domain capable of protecting cells against apoptosis. 10 Ability of HCV to prolong the life span of the cells it infects is believed to be of etiological significance, because it enhances the risk of accumulating genetic errors.

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Section: Discussionsupporting

confidence: 81%

HCV-Associated B Cell Clonalities in the Liver Do Not Carry the t(14;18) Chromosomal Translocation *

Sansonno

Tucci

et al. 2005

Hepatology

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“…These cells have been shown to express high levels of CD81 and to expand in HCV-infected liver. 67 Alternatively, B cells may need another event to become permissive for HCV infection or replication or both. This event could be coinfection with another virus.…”

Section: Evidence For An Oncogenic Role Of Hcv In Nhlmentioning

confidence: 99%

Hepatitis viruses and non-Hodgkin lymphoma: epidemiology, mechanisms of tumorigenesis, and therapeutic opportunities

Marcucci

Mele

2011

Blood

227

210

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Over the past 2 decades considerable evidence has accumulated on the association between hepatitis C virus (HCV) and hepatitis B virus (HBV) and several hematologic malignancies, most notably B-cell non-Hodgkin lymphoma (NHL). In this review we summarize this evidence, address possible mechanisms whereby hepatitis viruses may contribute to lymphomagenesis, and discuss the therapeutic fallouts from this knowledge. Most of this evidence is on HCV, and this is the main focus of the review. Moreover, we mainly address the association with NHL, the most prevalent hematologic malignancy, and the most extensively investigated with regard to an association with hepatitis viruses. Available evidence on the association with other hematologic malignancies is also addressed briefly. (Blood. 2011;117(6):1792-1798) Hepatitis C virus and hepatitis B virusHepatitis C virus (HCV) is a positive, single-stranded RNA virus, member of the Flaviviridae family. 1 During its replicative cycle it goes through a negative-stranded RNA, but not DNA, intermediate, so that integration of HCV nucleic acid sequences into the host genome seems unlikely. As such, it lacks a pivotal property of classical oncogenic retroviruses. The HCV genome produces a single polyprotein that is proteolytically processed by viral and cellular proteases to produce structural (nucleocapsid, E1, E2) and nonstructural (NS) proteins (NS2, NS3, NS4A, NS4B, NS5A, and NS5B).Hepatitis B virus (HBV) is a small DNA virus, member of the Hepadnaviridae family. 2 It presents the unusual feature, for a DNA virus, to replicate through a RNA intermediate and can integrate into the host genome. Moreover, during replication, it undergoes transformation into covalently closed circular DNA. Detection of closed circular DNA HBV-, or negative-stranded HCV-intermediates is important because it identifies genuine viral replication instead of more trivial events such as viral absorption. HBV is characterized by a genome consisting of 4 overlapping open-reading frames: the S gene, encoding envelope proteins; the core gene, encoding the core and "e" proteins; the P gene, encoding DNA polymerase; and the X gene, encoding a transcriptional transactivator.Both viruses can induce acute and chronic hepatitis and are strongly associated with hepatocellular carcinoma (HCC). Epidemiology of non-Hodgkin lymphomaNon-Hodgkin lymphoma (NHL) is the hematologic malignancy with the highest prevalence worldwide. Incidence rates have grown fast up to the beginning of the new millennium, with an annual percentage increase of nearly 3%, which is faster than for most cancers. Thus, delay-adjusted Surveillance, Epidemiology and End Results incidence rate for all races was 11.06/100 000 in 1975, and 20.12/100 000 in 2002. Since then, incidence rates have started to level off, at least in some geographic areas, such as the United States (20.89 in 2007). 3 NHL incidence rates are higher in developed countries such as those in western Europe, North America, and Australia and lower in South America and Asia, but th...

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“…Lastly, a process of viral antigen-specific stimulation can lead to B-cell activation and clonal expansion that promote both lymphomagenesis and autoimmunity [147,148]. For instance, HCV-associated lymphomas are often indolent [149] with frequent and varied autoimmune manifestations.…”

Section: Autoimmunity and Non-hodgkin Lymphomamentioning

confidence: 99%

Lymphoma-associated dysimmune polyneuropathies

Stübgen

2015

Journal of the Neurological Sciences

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Expansion of innate CD5pos B cells expressing high levels of CD81 in hepatitis C virus infected liver

Cited by 70 publications

References 48 publications

HCV-Associated B Cell Clonalities in the Liver Do Not Carry the t(14;18) Chromosomal Translocation *

HCV-Associated B Cell Clonalities in the Liver Do Not Carry the t(14;18) Chromosomal Translocation *

Hepatitis viruses and non-Hodgkin lymphoma: epidemiology, mechanisms of tumorigenesis, and therapeutic opportunities

Lymphoma-associated dysimmune polyneuropathies

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