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Hepatitis C Virus Genotype Distribution in B-Cell Non-Hodgkin Lymphoma
- Mario Luppi, MD;
- M. Grazia Ferrari, PhD; and
- Giuseppe Torelli, MD
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TO THE EDITOR:
Epidemiologic studies have shown hepatitis C virus (HCV) infection in a statistically significant proportion of de novo B-cell non-Hodgkin lymphomas that are not complicating the course of type II mixed cryoglobulinemia [1-3].
To study the influence of specific HCV genotypes on the pathogenesis of B-cell non-Hodgkin lymphoma, we analyzed 97 HCV-positive (anti-HCV antibody-positive and HCV RNA-positive) patients, including 35 patients with B-cell non-Hodgkin lymphoma that was not complicating the course of type II mixed cryoglobulinemia, 27 patients undergoing long-term hemodialysis, and 35 patients with chronic liver disease. The HCV genotype was determined by using a genotype-specific primer polymerase chain reaction method [4]. Results are summarized in the (Table 1). The prevalence of hepatitis C virus genotype 1b/II was unexpectedly lower in patients with B-cell non-Hodgkin lymphoma (25.7%) than in patients undergoing long-term hemodialysis (66.7%; P = 0.0013) and those with chronic liver disease (62.8%; P = 0.001). Conversely, the prevalence of genotypes 2a/III and 2b/IV was higher in patients with B-cell non-Hodgkin lymphoma (42.8%) than in the hemodialysis group (14.8%; P = 0.01) and chronic liver disease group (14.2%; P = 0.008).
The possible clinical relevance of the presence of different genotypes, in terms of prognosis or therapeutic response, in HCV-associated diseases has now emerged [5]. A high prevalence of genotype 2a/III in Italian patients who had cryoglobulinemia without associated liver disease but with circulating autoantibodies was recently reported; this finding suggests that this variant may have a pathogenetic role in autoimmune-lymphoproliferative disorders [4]. The different genotype distribution in our series of de novo B-cell non-Hodgkin lymphoma in comparison with patients undergoing hemodialysis and patients with chronic liver disease further supports the hypothesis that different HCV variants might be related to greater lymphotropism. Moreover, our observation indicates that HCV-related factors, namely viral genotypes, may play a role in the malignant proliferation of defined B-cell subsets, in addition to unknown host-related factors.
Mario Luppi, MD
M. Grazia Ferrari, PhD
Giuseppe Torelli, MD
University of Modena; 41100 Modena, Italy
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
- Copyright ©2004 by the American College of Physicians
