Contribution of Epstein–Barr Virus Latent Proteins to the Pathogenesis of Classical Hodgkin Lymphoma

Abstract

Pathogenic viruses have evolved to manipulate the host cell utilising a variety of strategies including expression of viral proteins to hijack or mimic the activity of cellular functions. DNA tumour viruses often establish latent infection in which no new virions are produced, characterized by the expression of a restricted repertoire of so-called latent viral genes. These latent genes serve to remodel cellular functions to ensure survival of the virus within host cells, often for the lifetime of the infected individual. However, under certain circumstances, virus infection may contribute to transformation of the host cell; this event is not a usual outcome of infection. Here, we review how the Epstein–Barr virus (EBV), the prototypic oncogenic human virus, modulates host cell functions, with a focus on the role of the EBV latent genes in classical Hodgkin lymphoma.

Dualism of Viruses in Oncology

“…Malignant lymphomas [47][48][49][50], Hodgkin lymphoma [51][52][53], Burkitt's lymphoma [54][55][56], gastric cancer [57][58][59], nasopharyngeal carcinoma [60][61][62], breast cancer [63,64], thyroid [65,66].…”

Signaling pathways of EBV-induced oncogenesis

“…The EBV genome encodes three latent membrane proteins (LMP1, LMP2A and LMP2B), five Epstein-Barr nuclear antigens (EBNA1, EBNA2, EBNA3A, EBNA3B and EBNA3C) and one leader protein (EBNA-LP). The EBV genome also encodes two different classes of miRNAs: Bam HI fragment H rightward open reading frame (BHRF1) miRNAs and BamHI-A rightward transcript (BART) miRNAs [ 2 ].…”

Novel Synthetic DNA Immunogens Targeting Latent Expressed Antigens of Epstein–Barr Virus Elicit Potent Cellular Responses and Inhibit Tumor Growth

“…The cancers associated with EBV are linked to their expression of EBV oncogenes, including Epstein–Barr virus nuclear antigen 1 (EBNA1) and latent membrane proteins 1 and 2 (LMP1 and LMP2) [14]. The latent viral oncoproteins of EBV are important cancer drivers and are implicated in directly contributing to EBV-associated malignancies [15,16,17].…”