Regulation of the latent-lytic switch in Epstein-Barr virus.
Epstein-Barr virus (EBV) infection contributes to the development of several different types of human malignancy, including Burkitt lymphoma, Hodgkin lymphoma, and nasopharyngeal carcinoma. As a herpesvirus, EBV can establish latent or lytic infection in cells. EBV-positive tumors are composed almost exclusively of cells with latent EBV infection. Strategies for inducing the lytic form of EBV infection in tumor cells are being investigated as a potential therapy for EBV-positive tumors. In this article, we review how cellular and viral proteins regulate the latent-lytic EBV switch in infected B cells and epithelial cells, and discuss how harnessing lytic viral reactivation might be used therapeutically.
McArdle Laboratory for Cancer Research, 1400 University Avenue, University of Wisconsin School of Medicine and Public Health, Madison, WI 53706-1599, USA; Department of Oncology, 1400 University Avenue, University of Wisconsin School of Medicine and Public Health, Madison, WI 53706-1599, USA; Department of Medicine, 1400 University Avenue, University of Wisconsin School of Medicine and Public Health, Madison, WI 53706-1599, USA. Electronic address: skenney@wisc.edu.
Shannon C
SC
Kenney
McArdle Laboratory for Cancer Research, 1400 University Avenue, University of Wisconsin School of Medicine and Public Health, Madison, WI 53706-1599, USA; Department of Oncology, 1400 University Avenue, University of Wisconsin School of Medicine and Public Health, Madison, WI 53706-1599, USA.
Janet E
JE
Mertz
D000818:Animals; D019175:DNA Methylation; D020031:Epstein-Barr Virus Infections / Q000821:virology*; D015967:Gene Expression Regulation, Viral; D016679:Genome, Viral; D004854:Herpesvirus 4, Human / Q000502:physiology*; D006801:Humans; D009369:Neoplasms / Q000628:therapy / Q000821:virology; D050130:Oncolytic Virotherapy; D050504:Oncolytic Viruses / Q000502:physiology; D014775:Virus Activation; D017735:Virus Latency; D014779:Virus Replication
Ataxia-telangiectasia mutated (ATM); Genome methylation; Hypoxia; Lytic induction therapy; TGF-β