Oncogenesis is a multifactorial process in which environmental, genetical and infectious factors may be of importance. Specific viruses are supposed to have etiological role in about 15% of human tumors. Recently the B-cell proliferation inducing effect of the hepatotropic and lymphotropic hepatitis-C virus (HCV) came into the limelight based on the high prevalence of HCV positivity in B-cell non-Hodgkin's lymphoma (NHL) patients. The aim of the authors was to establish the prevalence of HCV infection in NHL patients. Paralelly the HBV, CMV and EBV markers, and the alterations of the humoral immune response (immunoglobulins, cryoglobulins, rheumatoid factor) were determined. 42 patients (24 male, 18 female; the mean age: 54.1 years, range 22-80 years) classified as 16 indolent (low risk), and 25 aggressive (intermediate risk) NHL and one with very aggressive Burkitt's lymphoma, according to the modified REAL classification were examined. Enzyme-linked immunosorbent assay (ELISA) for HBsAg and anti-HCV, HBsAg, anti EBV, anti CMV, furthermore polymerase chain reaction (PCR) for HCV-RNA were used. Anti-HCV was found in 6/42 NHL patients (14.3%), while anti-HCV and/or HCV-RNA PCR positivity revealed on overall HCV infection in 10/42 (23.8%) patients. None of them were HBsAg positive. Our findings support the hypothesis, that HCV might have an aetiological role in the lymphoproliferation leading to B-cell NHL.
|Translated title of the contribution||Hepatitis C virus infection and B-cell non-Hodgkin's lymphoma|
|Number of pages||3|
|Publication status||Published - dec. 3 2000|
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