Abstract
Epstein-Barr virus (EBV) has been associated with several types of human cancers. In the host, EBV can establish two alternative modes of life cycle, known as latent or lytic and the switch from latency to the lytic cycle is known as EBV reactivation. Although EBV in cancer cells is found mostly in latency, a small number of lytically-infected cells promote carcinogenesis through the release of growth factors and oncogenic cytokines. This review focuses on the mechanisms by which EBV reactivation is controlled by cellular and viral factors, and discusses how EBV lytic infection contributes to human malignancies.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1309-1318 |
| Number of pages | 10 |
| Journal | International Journal of Biological Sciences |
| Volume | 12 |
| Issue number | 11 |
| DOIs | |
| State | Published - Oct 18 2016 |
Bibliographical note
Funding Information:This work was supported by the National Natural Science Foundation of China)(nos. 81161120410 and 81101474), the Innovation Foundation of Central South University (no.2013zzts072), and the Collaborative Innovation Center for Chemistry and Molecular Medicine of Hunan province, China.
Publisher Copyright:
© Ivyspring International Publisher.
Keywords
- Carcinogenesis
- Epstein-Barr virus
- Latency
- Reactivation
- Rta
- Zta
