Epigenetic Changes in Virus-Associated Neoplasms

Up-Regulation of Lamin A/C Expression in Epstein-Barr Virus Immortalized B Cells and Burkitt Lymphoma Cell Lines of Activated B Cell Phenotype

“…The expression of latent EBV genomes is highly restricted in Burkitt lymphoma (BL) cells that phenotypically resemble resting B cells: only EBNA1, an EBV-encoded nuclear antigen, and a set of non-translated viral RNAs can be detected [17]. The restricted EBV gene expression pattern characteristic of BLs in vivo and BL-derived cell lines that maintain the BL biopsy phenotype in vitro is called latency type I.…”

“…In addition to LMPs, however, six nuclear antigens (EBNAs) and three BHRF1 microRNAs are also expressed in latency type III [17,19,20]. It is worthy to note, that type III latency is also a characteristic of BL cells that acquired an activated B cell phenotype during in vitro cultivation.…”

Large-scale hypomethylated blocks associated with Epstein-Barr virus–induced B-cell immortalization

“…Although type III latency viral products (especially EBNA-2 and LMP-1) are essential to induce and maintain B-cell activation and proliferation, and several cellular pathways and genes targeted by these proteins have been described , the process of EBV-induced immortalization is still not well understood. Several observations, however, suggested that the epigenetic reprogramming of the host genome by viral products may play a central role in the process of immortalization (Niller et al 2012). …”

Patho-Epigenetics

“…It also became clear that viral oncoproteins, in addition to their interaction with various cellular signaling pathways, regularly interact with the cellular epigenetic machinery as well (epigenetic reprogramming). This topic has recently been reviewed [29,55], and here we only wish to highlight some special aspects of oncoprotein-induced epigenetic dysregulation. It seems that most key human oncoproteins, including human papillomavirus E7, Epstein-Barr virus LMP1, KSHV LANA, hepatitis C virus core protein, and hepatitis B virus HBx, can upregulate or stimulate the activity of at least one DNA methyltransferase enzyme, resulting in hypermethylation and silencing of certain cellular promoters (table 1).…”

“…Recently, it has been recognized that microbial pathogens could also dysregulate epigenetic mechanisms in their host cells (reviewed in Minarovits [14] and Niller et al [29,30]). The first human pathogen associated with the induction of patho-epigenetic alterations in host cells was, as far as we know, the human immunodeficiency virus (HIV), the causative agent of AIDS [31].…”