Hepatitis C virus genotypes and subtypes in patients with hepatitis C, with and without cryoglobulinemia

Frangeul, Lionel; Musset, Lucile; Cresta, Pascale; Cacoub, Patrice; Huraux, Jean‐Marie; Lunel, F.

doi:10.1016/s0168-8278(96)80200-5

Cited by 68 publications

(45 citation statements)

References 22 publications

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“…Differences in the population and viral genotype might also explain the different values for ANCA in our study (24%) compared to another study, in which 60% of patients with chronic active hepatitis were positive. 43 A lower prevalence of cryoglobulins in our study in comparison to those previously reported 44 could be related to regional differences or the stage of liver disease, as suggested by others. 45 Treatment may influence the picture of autoantibody profile.…”

Section: Discussionsupporting

confidence: 55%

Prevalence of Autoantibodies in Patients with Hepatitis C Virus Infection in Oman

Alnaqdy¹,

Alfahdi²,

Al-Kobaisi³

et al. 2003

Ann Saudi Med

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Background: HCV genotype patterns and HLA types in the Omani population may be unique. Subjects and Methods: Tests for 12 different autoantibodies were carried out on 50 HCV-infected patients and on 27 HCV-seronegative controls. An immunoassay for the detection of anti-HCV antibodies was performed on patient and control sera. HCV PCR was carried out on those sera which were positive for HCV antibodies. Results: All patients' sera were positive for HCV antibodies and all control sera were negative. Sixty-six percent of patients were positive for at least one autoantibody. In contrast, only 33% of the controls showed positivity for one or more autoantibodies. Conclusion: This study found a significant difference in the prevalence of autoantibodies between patients and controls, and between organ-and non-organ specific autoantibodies among the patients. A comparison with autoantibody patterns reported for HCV-infected patients in other parts of the world suggest that patterns in HCVinfected individuals in the Omani population are unique.

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Section: Discussionsupporting

confidence: 55%

Prevalence of Autoantibodies in Patients with Hepatitis C Virus Infection in Oman

Alnaqdy¹,

Alfahdi²,

Al-Kobaisi³

et al. 2003

Ann Saudi Med

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“…Discordance among different studies may be influenced by geographical factors as well as by the different criteria used in population selection. 1,29 In some studies, a high frequency of type 2a/c was detected in HCV-related LPDs including type II MC, B-cell NHL, and monoclonal gammopathies. 1,4,30,31 In light of present and past observations, it is possible that different viral types exert a lesser or more important influence on favoring the appearance of LPDs.…”

Section: Discussionmentioning

confidence: 99%

T(14;18) translocation in chronic hepatitis C virus infection

et al. 2000

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Pathogenic mechanisms of B-cell lymphoproliferative disorders in chronic hepatitis C virus (HCV) infection are unclear. We studied t(14;18) translocation by polymerase chain reaction in peripheral blood mononuclear cells from 50 patients with HCV-related liver disease (group A), 7 with mixed cryoglobulinemia syndrome (group B), 55 with HCV-negative liver disease (group C), and 30 with HCVnegative chronic rheumatic disorders or chronic infection by nonhepatotropic agents (group D). T(14;18) was significantly more frequent in group A (13/50 patients ‫؍‬ 26 %) and group B (5/7 ‫؍‬ 71.4%) patients than in group C (1/55 ‫؍‬ 3.6%) and group D (1/30 ‫؍‬ 3.3%) ones. Immunoblot analysis showed bcl-2 over-expression in all t(14;18)-positive samples. In group A, 10/13 (77%) patients with t(14;18) and 13/37 (35%) without t(14;18) had serum cryoglobulins in the absence of mixed cryoglobulinemia symptoms (P F .05). These data indicate that t(14;18) and bcl-2 over-expression in lymphoid cells are frequent in chronic HCV infection and suggest that this event may contribute to the pathogenesis of HCV-related lymphoproliferative disorders. (HEPATOLOGY 2000;31:474-479.)Hepatitis C virus (HCV) infection has been associated with a series of B-cell lymphoproliferative disorders (LPDs), including essential mixed cryoglobulinemia (MC), B-cell non-Hodgkin' s lymphoma (NHL), and monoclonal gammopathies. [1][2][3][4] The mechanisms involved in LPDs, either virusrelated or virus-independent, are complex and still poorly defined. MC, the LPD most strictly associated with HCV infection, is a borderline (benign/malignant) disorder in that it frequently coexists with bone-marrow aspects of NHL and evolves, in about 5% to 8% of cases, into a clinically frank B-cell malignancy. 5,6 In addition, clonal expansion of IgMproducing B cells has been detected in patients with HCVpositive MC (HCV/MC). 7 Recently, 1 patient with HCV/MC has been shown to develop a monoclonal multistep lymphoproliferative disorder associated with t(14;18) translocation in the benign phase of the disease and additional genetic alterations in the accelerated one. 8 Over-expression of bcl-2 oncoprotein has been shown by immunohistochemistry in liver lymphocyte aggregates not only in the majority of HCV-positive MC, but also in about 45% of patients with chronic HCV-related hepatitis without MC. 9 The recombination of anti-apoptotic bcl-2 proto-oncogene [t(14;18)] has been widely investigated in the field of lymphomagenetic studies. Following t(14;18), the bcl-2 locus, normally located in chromosome 18, is juxtaposed with the immunoglobulin heavy chain locus (IgH), leading to bcl-2 activation. This genetic aberration, which occurs during early B-cell development, appears to be 1 step toward the progression of a normal cell to a cancer cell 10 ; in particular, its importance in regards to cooperative activities with different oncogenes, such as c-myc, has been experimentally shown. T(14;18) characterizes most follicular B-cell lymphomas as well as some diffuse ones. Recent data...

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“…Activation of the cytokine network is triggered in human B-cells in response to HCV RNA. In fact, host factors liberated by HCV-infecting B-cells have been previously reported in HCV patients (1,12,15,16,52). Although patients' outcomes would be more than we can be predicted from our results, this system would actually benefit the future study on B-cell-virus interaction.…”

Section: Fig 2 J6jfh1 B-cell Infection Is Blocked By Anti-cd81mentioning

confidence: 62%

“…Chronic hepatitis patients with HCV sometimes show other extrahepatic complications such as lymphoproliferative diseases (LPD), including cryoglobulinemia and B-cell malignant lymphoma, autoimmune diseases, and dermatitis (1,12,15,16). Epidemiological analysis shows that chronic HCV patients have higher rates of LPDs than non-HCVinfected populations (36,48,52).…”

mentioning

confidence: 99%

The J6JFH1 Strain of Hepatitis C Virus Infects Human B-Cells with Low Replication Efficacy

et al. 2014

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Hepatitis C virus (HCV) infection is a serious health problem worldwide that can lead to hepatocellular carcinoma or end-stage liver disease. Current treatment with pegylated interferon, ribavirin, and NS3/4A protease inhibitor would lead to a good prognosis in a large population of patients, but there is still no effective vaccine for HCV. HCV robustly infects hepatocytes in the liver. However, extrahepatic manifestations such as mixed cryoglobulinemia, a systemic immune complex-mediated disorder characterized by B-cell proliferation, which may evolve into overt B-cell non-Hodgkin's lymphoma, have been demonstrated. HCV-RNA is often found to be associated with peripheral blood lymphocytes, suggesting a possible interaction with peripheral blood mononuclear cells (PBMCs), especially B-cells with HCV. B-cell HCV infection was a matter of debate for a long time, and the new advance in HCV in vitro infectious systems suggest that exosome can transmit HCV genome to support ''infection.'' We aimed to clarify the susceptibility of primary B-cells to HCV infection, and to study its functional effect. In this article, we found that the recombinant HCV J6JFH1 strain could infect human B-cells isolated from the peripheral blood of normal volunteers by the detection of both HCV-negative-strand RNA by reverse transcription polymerase chain reaction, and NS5A protein. We also show the blocking of HCV replication by type I interferon after B-cell HCV infection. Although HCV replication in B-lymphocytes showed lower efficiency, in comparison with hepatocyte line (Huh7) cells, our results clearly demonstrate that human Blymphocytes without other non-B-cells can actually be infected with HCV, and that this interaction leads to the induction of B-cells' innate immune response, and change the response of these cells to apoptosis.

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Hepatitis C virus genotypes and subtypes in patients with hepatitis C, with and without cryoglobulinemia

Cited by 68 publications

References 22 publications

Prevalence of Autoantibodies in Patients with Hepatitis C Virus Infection in Oman

Prevalence of Autoantibodies in Patients with Hepatitis C Virus Infection in Oman

T(14;18) translocation in chronic hepatitis C virus infection

The J6JFH1 Strain of Hepatitis C Virus Infects Human B-Cells with Low Replication Efficacy

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