Infection of peripheral mononuclear blood cells by hepatitis C virus

Zignego, Anna Linda; Macchia, Donatella; Monti, Monica; Thiers, Valérie; Mazzetti, Marcello; Foschi, Marco; Maggi, Enrico; Romagnani, Sergio; Geñtilini, Paolo; Bréchot, Christian

doi:10.1016/0168-8278(92)90073-x

Cited by 409 publications

(237 citation statements)

References 9 publications

Supporting

Mentioning

221

Contrasting

Unclassified

Order By: Relevance

“…[16][17][18][19] On the contrary, genotype 2a is more likely to be found among apparently healthy blood donors than in patients with CLD, 32 or in patients with mild CLD or in those who respond better to IFN therapy. [12][13][14][15][16][17][18][19] HCV might be a causative cofactor in the pathogenesis of B cell NHL: it is found in a significative percentage of some histotypes of NHL, 8,11,33,34 it is known to be able to infect B lymphocytes circulating in the peripheral blood (PB) 35 or infiltrating the bone marrow (BM) 36 and the liver, 37 and in vitro studies have shown its ability to infect a human BM-derived B cell line and the PB MNC from healthy subjects. [38][39][40] If this is the case, it would appear appropriate to assess the prevalence of different HCV genotypes among the patients bearing a B cell NHL, with the aim of finding a possible correlation between a particular genotype and the lympho-proliferative disorder.…”

Section: Discussionmentioning

confidence: 99%

The genotype of the hepatitis C virus in patients with HCV-related B cell non-Hodgkin’s lymphoma

et al. 1997

View full text Add to dashboard Cite

Increasing evidence suggests that the hepatitis C virus (HCV) might be involved in the pathogenesis of B cell non-Hodgkin's lymphomas (NHL). Since several HCV genotypes are currently identifiable and might be involved in the pathogenesis of different diseases (with different severity and responsiveness to therapy), the aim of our study was to assess the prevalence of viral genotypes in a group of patients with HCV-related NHL. Among 470 consecutive patients, 42 HCV Ab-positive cases were identified. HCV RNA could be detected by reverse transcriptase-polymerase chain reaction and genotyping performed in 31 of these cases. As compared to our control group (211 healthy blood donors and patients with chronic liver disease), a striking high prevalence of genotype 2ac was detected among B cell NHL (48.4 vs 9.0%), with a relative risk of infection of 5.37 (P Ͻ 0.0001). No major differences were observed in the distribution of NHL histotypes and in the clinical features among patients with genotype 1b (the other most frequent genotype) or 2ac, a part from a trend towards a higher percentage of liver disease and a lower likelihood of response to interferon for patients with genotype 1b. The same high prevalence of genotype 2ac has been recently reported in patients with mixed cryoglobulinemia (MC), monoclonal gammopathies, B cell NHL complicating MC and autoimmune hepatitis. All these data taken together suggest that genotype 2ac might be involved in the pathogenesis of lymphoproliferative and autoimmune disorders.

show abstract

Section: Discussionmentioning

confidence: 99%

The genotype of the hepatitis C virus in patients with HCV-related B cell non-Hodgkin’s lymphoma

et al. 1997

View full text Add to dashboard Cite

show abstract

“…In addition to its being hepatotrophic, HCV is also a lymphotrophic virus [2]. This peculiar lymphotropism may be responsible, at least in part, for the multiple immune-mediated extra hepatic manifestations of HCV infection, such as mixed cryoglobulinaemia [3][4][5], Sjögren-like syndrome [6], the presence of serum rheumatoid factor (RF), the production of autoantibodies [7][8][9][10][11] and B-cell non-Hodgkin lymphoma [12][13][14].…”

Section: Introductionmentioning

confidence: 99%

Peripheral B-cell CD5 expansion and CD81 overexpression and their association with disease severity and autoimmune markers in chronic hepatitis C virus infection

Zuckerman¹,

Slobodin²,

Kessel

et al. 2002

Clinical and Experimental Immunology

View full text Add to dashboard Cite

SUMMARYHepatitis C virus (HCV) infection is associated with immune-mediated abnormalities and B-cell lymphoproliferation evolving to an overt lymphoma. Recently, CD81 was identified as an HCV receptor on B-lymphocytes, providing a mechanism by which B cells are infected and activated by the virus. In addition, expansion of CD5 + B lymphocytes was described to be associated with various non-HCV related autoimmune disorders. Therefore, we studied the possible role of peripheral B cells CD81 and CD5 over-expression in the development of HCV-related autoimmunity and their association with disease severity in chronic HCV infection. Peripheral B cells CD5 expression and mean fluorescence intensity (MFI) of CD81 were determined in 30 HCV-infected patients, 30 healthy controls and 15 patients with hepatitis B virus infection using fluorescence-activated cell scan (FACS). We have also investigated the association between peripheral CD5 and CD81 B-cell over-expression and markers of autoimmunity and disease severity in patients chronically infected by HCV. CD5 + B-cells were increased in chronic HCV infection (23·2 ± 7·2%) compared with those of healthy controls (15 ± 5·5%) (P < 0·0001) and chronic HBV infection (19 ± 3·7%) (P = 0·08). CD81 MFI was significantly higher in HCVinfected compared to HBV-infected patients and healthy controls. Both increased CD81 MFI and CD5 + B-cell expansion were associated with the production of rheumatoid factor and mixed cryoglobulins and positively correlated with HCV viral load and histological activity index. The overexpression of CD81 and the expansion of CD5 + peripheral B-cells in HCV-infected patients may possibly play a role in the development of HCV-associated autoimmunity and lymphoproliferation.

show abstract

“…6). HCV has been recognized to be both a hepatoand lymphotropic virus, as suggested by the presence of active or latent viral replication in the peripheral lymphocytes of patients with type C hepatitis or MC [3,73,77]. HCV is an RNA virus without reverse trascriptase activity; therefore viral genome cannot integrate in the host genome [63].…”

Section: Etiopathogenesismentioning

confidence: 99%

“…6). This latter may in turn favors the apparition of t [14,18] translocation and Bcl-2 overexpression; the consequent B-lymphocyte expansion is responsible for autoantibody production, including the cryoglobulins [3,11,12,63,[77][78][79]. In addition, the prolonged B cell survival may represent a predisposing condition for further genetic aberrations, which may lead to frank B-cell malignancy as late complication of MC syndrome [11,20,24,82].…”

Section: Etiopathogenesismentioning

confidence: 99%