The human bone-marrow-derived B-cell line CE, susceptible to hepatitis C virus infection

Bertolini, Luisa; Iacovacci, S.; Ponzetto, Antonio; Gorini, Giovanni; Battaglia, Martina; Carloni, Guido

doi:10.1016/s0923-2516(06)80041-5

Cited by 72 publications

(35 citation statements)

References 6 publications

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“…[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

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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.

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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

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“…Humans and other primates are the only known hosts for HCV infection. Furthermore, only a limited number of cell lines can support HCV replication (30)(31)(32)(33). Viral replication in these cells, however, is unstable, and the viral titers can be measured only by PCR.…”

Section: Discussionmentioning

confidence: 99%

Intracellular cleavage of hepatitis C virus RNA and inhibition of viral protein translation by hammerhead ribozymes.

Sakamoto¹,

Wu²,

Wu³

1996

J. Clin. Invest.

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To determine the effects of hammerhead ribozymes against hepatitis C virus (HCV) RNA on viral protein translation, a luciferase reporter gene vector, pCMV/T7-NCRC ⌬ -luc, was constructed containing the 5 Ј -noncoding region (5 Ј -NCR) and part of the core region of HCV. Four ribozymes, Rz1-Rz4, were designed to cleave at nucleotide positions 136-160, 313-337, 496-520, and 373-388, respectively. Each ribozyme cleaved the target RNA at expected positions under cell-free conditions. Rz2 and Rz4 significantly suppressed translation of NCRC ⌬ -luc RNA by 71 and 49%, respectively. Translation of control luciferase mRNA lacking viral elements was not affected by the ribozymes. Furthermore, when NCRC ⌬ -luc RNA and ribozymes were cotransfected into cells, Rz2 and Rz4 significantly suppressed expression by 73 and 56%, respectively. In contrast, cleavage-deficient ribozymes with a point mutation in the hammerhead domain had no significant effect. To determine the effects of endogenously produced ribozymes, eukaryotic expression vectors for Rz2 and Rz4 were constructed. Cotransfection of the vectors with CMV/T7-NCRC ⌬ -luc showed suppression of luciferase activities to 50 and 61%, respectively. Moreover, transfection of pCMV/T7-NCRC ⌬ -luc into stable Rz2 and Rz4 producer cells also showed substantial inhibition of luciferase activity. Ribozymes directed against the HCV genome can substantially and specifically inhibit viral gene expression under intracellular conditions. ( J. Clin. Invest. 1996. 98:2720-2728.)

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“…Despite recent progress made in this direction, efforts in developing a cell culture system susceptible to infection and permissive for replication of HCV remain a priority. In vitro culture systems for HCV infection have been described for peripheral blood mononuclear cells (Bouffard et al, 1992 ;Zignego et al, 1992 ;Mu$ ller et al, 1993 ;Willems et al, 1994 ;Cribier et al, 1995), human B and T cell lines (Shimizu et al, 1992(Shimizu et al, , 1993Bertolini et al, 1993 ;Shimizu & Yoshikura, 1994 ;Kato et al, 1995 ;Nakajima et al, 1996) and human hepatocyte cell lines (Tagawa et al, 1995 ;Kato et al, 1996 ;Seipp et al, 1997). Efficient long term in vitro replication has not been demonstrated and the results obtained with conventional RT-PCR assays for detection of replicating viral RNA must be interpreted with care (Willems et al, 1993 ;Lanford et al, 1994 ;McGuiness et al, 1994 ;Lerat et al, 1996 ;Laskus et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

In vitro infection of adult normal human hepatocytes in primary culture by hepatitis C virus.

Fournier

Sureau

Coste

et al. 1998

Journal of General Virology

120

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In vitro infection of adult normal human hepatocytes in primary culture has been performed for investigating the replication cycle of hepatitis C virus (HCV) in differentiated cells. Hepatocytes were prepared from liver tissue resected from donors who tested negative for HCV, and inoculation was performed 3 days after plating with 33 HCV serum samples of different virus load and genotype. The presence of intracellular HCV RNA, detected by a strand-specific rTth RT-PCR assay, was used as evidence of infection. A kinetics analysis of HCV replication revealed that intracellular negative-strand RNA appeared at day 1 post-infection with a maximum level at days 3 and 5, followed by a decrease until

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The human bone-marrow-derived B-cell line CE, susceptible to hepatitis C virus infection

Cited by 72 publications

References 6 publications

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

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

Intracellular cleavage of hepatitis C virus RNA and inhibition of viral protein translation by hammerhead ribozymes.

In vitro infection of adult normal human hepatocytes in primary culture by hepatitis C virus.

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