| First Author | Yasuda T | Year | 2013 |
| Journal | Cold Spring Harb Symp Quant Biol | Volume | 78 |
| Pages | 259-63 | PubMed ID | 24241423 |
| Mgi Jnum | J:217520 | Mgi Id | MGI:5614315 |
| Doi | 10.1101/sqb.2013.78.020222 | Citation | Yasuda T, et al. (2013) Studying Epstein-Barr virus pathologies and immune surveillance by reconstructing EBV infection in mice. Cold Spring Harb Symp Quant Biol 78:259-63 |
| abstractText | Epstein-Barr virus (EBV) is a gamma herpes virus endemic in humans and transforming human B lymphocytes. It causes a variety of human pathologies ranging from infectious mononucleosis upon acute infection to EBV-driven B-cell lymphomas. In humans, EBV-infected cells are under powerful immune surveillance by T and NK cells. If this immune surveillance is compromised as in immunosuppressed (AIDS- or posttransplantation) patients, the virus can spread from rare, EBV-containing cells and cause life-threatening pathologies. We have found that EBV immune surveillance and lymphomagenesis can be modeled in mice by targeted expression of key EBV proteins in the B-cell lineage. As EBV does not infect mouse B cells and mice have thus not coevolved with the virus, EBV exploits basic modes of the host immune response to optimize its coexistence with the host. |
