| First Author | Kasama Y | Year | 2010 |
| Journal | Blood | Volume | 116 |
| Issue | 23 | Pages | 4926-33 |
| PubMed ID | 20733156 | Mgi Jnum | J:167427 |
| Mgi Id | MGI:4868197 | Doi | 10.1182/blood-2010-05-283358 |
| Citation | Kasama Y, et al. (2010) Persistent expression of the full genome of hepatitis C virus in B cells induces spontaneous development of B-cell lymphomas in vivo. Blood 116(23):4926-33 |
| abstractText | Extrahepatic manifestations of hepatitis C virus (HCV) infection occur in 40%-70% of HCV-infected patients. B-cell non-Hodgkin lymphoma is a typical extrahepatic manifestation frequently associated with HCV infection. The mechanism by which HCV infection of B cells leads to lymphoma remains unclear. Here we established HCV transgenic mice that express the full HCV genome in B cells (RzCD19Cre mice) and observed a 25.0% incidence of diffuse large B-cell non-Hodgkin lymphomas (22.2% in males and 29.6% in females) within 600 days after birth. Expression levels of aspartate aminotransferase and alanine aminotransferase, as well as 32 different cytokines, chemokines and growth factors, were examined. The incidence of B-cell lymphoma was significantly correlated with only the level of soluble interleukin-2 receptor alpha subunit (sIL-2Ralpha) in RzCD19Cre mouse serum. All RzCD19Cre mice with substantially elevated serum sIL-2Ralpha levels (> 1000 pg/mL) developed B-cell lymphomas. Moreover, compared with tissues from control animals, the B-cell lymphoma tissues of RzCD19Cre mice expressed significantly higher levels of IL-2Ralpha. We show that the expression of HCV in B cells promotes non-Hodgkin-type diffuse B-cell lymphoma, and therefore, the RzCD19Cre mouse is a powerful model to study the mechanisms related to the development of HCV-associated B-cell lymphoma. |
