Abstract
Emerging evidences indicate that hepatitis B virus (HBV) infection is associated with non-Hodgkin lymphoma (NHL), but the mechanisms of HBV-induction lymphomagenesis remain unclear. In this report, retrospective analysis of the prevalence of hepatitis B surface antigen (HBsAg) among NHL cases demonstrated significantly higher HBsAg carrier rate among B-cell NHL cases than controls (other cancers except primary liver cancer) (adjusted odds ratio, 1.56; 95% confidence interval, 1.13–2.16). Furthermore, cells with an immortalization potential existed in the peripheral blood of 4 patients with chronic HBV infection. Characterization of these cells showed their immunophenotypes similar to that of the majority of HBsAg-positive B-cell NHL patients. Immunoglobulin (Ig) gene rearrangements confirmed the clonal Ig gene rearrangements. Cytogenetic analysis revealed abnormal karyotypes of these cells with an immortalization potential. Compared with cells with an immortalization potential that we previously found in B-cell NHL patients by the same way, these cells showed many similar features. In conclusion, cells with an immortalization potential existed in the part of patients with chronic HBV infection before lymphoma development and showed some malignant features. They may be the cellular basis of HBV-associated lymphomagenesis.
Highlights
Non-Hodgkin lymphoma (NHL) is a common hematological malignancy
Mechanisms of NHL development are very complex and the virus infection plays an important role in lymphomagenesis such as Epstein-Barr virus (EBV), hepatitis B virus (HBV), hepatitis C virus (HCV), human immunodeficiency virus (HIV) and herpes virus-8 (HHV-8) [2]
Carrier rates of hepatitis B surface antigen (HBsAg) among B-cell NHL patients were significantly higher than the control group (10.8%) (P = 0.001, adjusted odds ratio, 1.56; 95% confidence interval, 1.13–2.16) after adjusted for sex and age
Summary
About 509,590 new cases of NHL and 248,724 deaths are estimated to have occurred in 2018 worldwide[1]. Mechanisms of NHL development are very complex and the virus infection plays an important role in lymphomagenesis such as Epstein-Barr virus (EBV), hepatitis B virus (HBV), hepatitis C virus (HCV), human immunodeficiency virus (HIV) and herpes virus-8 (HHV-8) [2]. The International Agency for Research on Cancer (IARC) has identified HBV as a risk factor for NHL [3]. Individuals with chronic HBV infection have about 2.8 folds higher risk of NHL than comparison persons [4]. There are estimated about 257 million persons living with HBV infection in 2015 worldwide [5]. HBV infection was endemic in China, where there are 120
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