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

Salvatore De Vita, Valli De Re, Domenico Sansonno, Annunziata Gloghini, Daniela Gasparotto, Massimo Libra, Stefania Sacco, Antonino Carbone, Gianfranco Ferraccioli, Mauro Boiocchi

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)400-406
Number of pages7
JournalTumori
Volume88
Issue number5
Publication statusPublished - Sep 2002

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B-Cell Lymphoma
Virus Diseases
Hepacivirus
Non-Hodgkin's Lymphoma
Viruses
B-Lymphocytes
Cryoglobulinemia
Polymerase Chain Reaction
Immunoglobulin Genes
Viral Genome
Infection
In Situ Hybridization
Immunohistochemistry
Antigens

Keywords

  • B-cell NHL
  • Cryoglobulinemia
  • HCV
  • IgR

ASJC Scopus subject areas

  • Cancer Research

Cite this

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. / De Vita, Salvatore; De Re, Valli; Sansonno, Domenico; Gloghini, Annunziata; Gasparotto, Daniela; Libra, Massimo; Sacco, Stefania; Carbone, Antonino; Ferraccioli, Gianfranco; Boiocchi, Mauro.

In: Tumori, Vol. 88, No. 5, 09.2002, p. 400-406.

Research output: Contribution to journalArticle

De Vita, S, De Re, V, Sansonno, D, Gloghini, A, Gasparotto, D, Libra, M, Sacco, S, Carbone, A, Ferraccioli, G & Boiocchi, M 2002, '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', Tumori, vol. 88, no. 5, pp. 400-406.
De Vita, Salvatore ; De Re, Valli ; Sansonno, Domenico ; Gloghini, Annunziata ; Gasparotto, Daniela ; Libra, Massimo ; Sacco, Stefania ; Carbone, Antonino ; Ferraccioli, Gianfranco ; Boiocchi, Mauro. / 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. In: Tumori. 2002 ; Vol. 88, No. 5. pp. 400-406.
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AU - Libra, Massimo

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