Header

UZH-Logo

Maintenance Infos

Latency and lytic replication in Epstein-Barr virus-associated oncogenesis


Münz, Christian (2019). Latency and lytic replication in Epstein-Barr virus-associated oncogenesis. Nature Reviews. Microbiology, 17(11):691-700.

Abstract

Epstein-Barr virus (EBV) was the first tumour virus identified in humans. The virus is primarily associated with lymphomas and epithelial cell cancers. These tumours express latent EBV antigens and the oncogenic potential of individual latent EBV proteins has been extensively explored. Nevertheless, it was presumed that the pro-proliferative and anti-apoptotic functions of these oncogenes allow the virus to persist in humans; however, recent evidence suggests that cellular transformation is not required for virus maintenance. Vice versa, lytic EBV replication was assumed to destroy latently infected cells and thereby inhibit tumorigenesis, but at least the initiation of the lytic cycle has now been shown to support EBV-driven malignancies. In addition to these changes in the roles of latent and lytic EBV proteins during tumorigenesis, the function of non-coding RNAs has become clearer, suggesting that they might mainly mediate immune escape rather than cellular transformation. In this Review, these recent findings will be discussed with respect to the role of EBV-encoded oncogenes in viral persistence and the contributions of lytic replication as well as non-coding RNAs in virus-driven tumour formation. Accordingly, early lytic EBV antigens and attenuated viruses without oncogenes and microRNAs could be harnessed for immunotherapies and vaccination.

Abstract

Epstein-Barr virus (EBV) was the first tumour virus identified in humans. The virus is primarily associated with lymphomas and epithelial cell cancers. These tumours express latent EBV antigens and the oncogenic potential of individual latent EBV proteins has been extensively explored. Nevertheless, it was presumed that the pro-proliferative and anti-apoptotic functions of these oncogenes allow the virus to persist in humans; however, recent evidence suggests that cellular transformation is not required for virus maintenance. Vice versa, lytic EBV replication was assumed to destroy latently infected cells and thereby inhibit tumorigenesis, but at least the initiation of the lytic cycle has now been shown to support EBV-driven malignancies. In addition to these changes in the roles of latent and lytic EBV proteins during tumorigenesis, the function of non-coding RNAs has become clearer, suggesting that they might mainly mediate immune escape rather than cellular transformation. In this Review, these recent findings will be discussed with respect to the role of EBV-encoded oncogenes in viral persistence and the contributions of lytic replication as well as non-coding RNAs in virus-driven tumour formation. Accordingly, early lytic EBV antigens and attenuated viruses without oncogenes and microRNAs could be harnessed for immunotherapies and vaccination.

Statistics

Citations

Dimensions.ai Metrics
10 citations in Web of Science®
9 citations in Scopus®
Google Scholar™

Altmetrics

Downloads

64 downloads since deposited on 07 Feb 2020
64 downloads since 12 months
Detailed statistics

Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > Institute of Experimental Immunology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Scopus Subject Areas:Life Sciences > Microbiology
Life Sciences > General Immunology and Microbiology
Health Sciences > Infectious Diseases
Language:English
Date:November 2019
Deposited On:07 Feb 2020 13:50
Last Modified:29 Jul 2020 13:51
Publisher:Nature Publishing Group
ISSN:1740-1526
OA Status:Green
Publisher DOI:https://doi.org/10.1038/s41579-019-0249-7
PubMed ID:31477887

Download

Green Open Access

Download PDF  'Latency and lytic replication in Epstein-Barr virus-associated oncogenesis'.
Preview
Content: Accepted Version
Filetype: PDF
Size: 763kB
View at publisher