Deregulation of the cell cycle machinery by Epstein––Barr virus nuclear antigen 3C. (January 2009)

• Record Type: Journal Article
• Authors: Kumar, Pankaj; Murakami, Masanao; Kaul, Rajeev; Saha, Abhik; Cai, Qiliang; Robertson, Erle S
• Is Part Of: Future virology. Volume 4:Number 1(2009)
• Page Start: 79
• Page End: 91
• Publication Date: 2009-01
• Subjects: cell cycle -- Epstein––Barr nuclear antigen 3C -- Epstein––Barr virus -- latency -- transcriptional regulator -- viral transformation; Virology -- Periodicals; Virus diseases -- Treatment -- Periodicals; 616.9101
• DOI: 10.2217/17460794.4.1.79
• Languages: English
• ISSNs: 1746-0794

Abstract

Epstein––Barr virus (EBV) is a ubiquitous human herpesvirus associated with a large number of lymphoid and epithelial malignancies. As a successful pathogen it has co-evolved with its human host for millions of years. EBV has the unique ability to establish life-long latent infection in primary human B lymphocytes. During latent infection, a small subset of viral proteins is expressed. These proteins are essential for maintenance of the EBV genome as well as the deregulation of various signaling pathways that facilitate the proliferation and survival of the infected cells. Epstein––Barr nuclear antigen (EBNA)3C is one of the latent proteins shown to be essential for transformation of primary human B lymphocytes in vitro . EBNA3C primarily functions as a transcriptional regulator by interacting with a number of well known cellular and viral transcriptional factors. We have recently identified several binding partners for EBNA3C including proteins that regulate cell cycle and chromatin remodeling. We are actively engaged in discerning the biological significance of these interactions. This review summarizes our current understanding of how EBNA3C usurps cellular pathways that promote B-cell transformation.