Molecular Basis of Epstein–Barr Virus Latency Establishment and Lytic Reactivation

Viruses

Atsuko Sugimoto¹  Takayuki Murata¹  Tomoki Inagaki²  Yoshitaka Sato²  Yusuke Yanagi²  Hiroshi Kimura²  Takahiro Watanabe² 

[1] Department of Virology and Parasitology, Fujita Health University School of Medicine, Toyoake 470-1192, Japan;Department of Virology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan;

关键词: EBV;    latency;    reactivation;    transcription;    epigenetics;    oncogenesis;   

DOI  :  10.3390/v13122344

来源: DOAJ

【 摘 要 】

Epstein–Barr virus (EBV) is a causative agent of infectious mononucleosis and several types of cancer. Like other herpesviruses, it establishes an asymptomatic, life-long latent infection, with occasional reactivation and shedding of progeny viruses. During latency, EBV expresses a small number of viral genes, and exists as an episome in the host–cell nucleus. Expression patterns of latency genes are dependent on the cell type, time after infection, and milieu of the cell (e.g., germinal center or peripheral blood). Upon lytic induction, expression of the viral immediate-early genes, BZLF1 and BRLF1, are induced, followed by early gene expression, viral DNA replication, late gene expression, and maturation and egress of progeny virions. Furthermore, EBV reactivation involves more than just progeny production. The EBV life cycle is regulated by signal transduction, transcription factors, promoter sequences, epigenetics, and the 3D structure of the genome. In this article, the molecular basis of EBV latency establishment and reactivation is summarized.

【 授权许可】

Unknown