Epstein Barr Virus Associated Lymphomas and Epithelia Cancers in Humans

Abstract

Epstein Barr virus (EBV) is a cosmopolitan oncogenic virus, infecting about 90% of the world's population and it is associated to tumors originating from both epithelia and hematopoietic cells. Transmission of the virus is mainly through oral secretions; however, transmission through organ transplantation and blood transfusion has been reported. In order to evade immune recognition, EBV establishes latent infection in B lymphocytes where it expresses limited sets of proteins called EBV transcription programs (ETPs), including six nuclear antigens (EBNAs), three latent membrane proteins (LMP), and untranslated RNA called EBV encoded RNA (EBER), shown to efficiently transform B cells into lymphoblastic cells. These programs undergo different patterns of expression which determine the occurrence of distinct types of latency in the pathogenesis of a particular tumor. Hematopoietic cell derived tumors include but not limited to Burkitt's lymphoma, Hodgkin lymphoma, post-transplant lymphoproliferative disorders, and natural killer (NK)/T cell lymphoma. EBV undergoes lytic infection in epithelia cells for amplification of the viral particle for transmission where it expresses lytic stage genes. However, for reasons yet to be unveiled, EBV switches from the expression of lytic stage genes to the expression of ETPs in epithelia cells. The expression of the ETPs lead to the transformation of epithelia cells into permanently proliferating cells, resulting in epithelia cell derived malignancies such as nasopharyngeal cancer, gastric cancer, and breast cancer. In this review, we have summarized the current updates on EBV associated epithelial and B cell-derived malignancies, and the role of EBV latency gene products in the pathogenesis of the cancers, and have suggested areas for future studies when considering therapeutic measures

High-Risk Human Papillomaviruses and Epstein–Barr Virus in Colorectal Cancer and Their Association with Clinicopathological Status

“…This in turn leads to transcriptional activation of viral LMP genes (LMP-1 and -2) promoting cellular proliferation [ 45 , 46 , 47 ]. During latency 0, no EBNA protein is expressed, while only one EBNA (EBNA1) is expressed during latency I and II, and during latency III, all six EBNAs are expressed [ 48 , 49 , 50 ]. Further, the co-presence of both EBNA1 and LMP1 in our cohort can be explained by the fact that in EBV-infected cells, in the latent phase, EBNA1 and LMP1 are expressed in a cancer-specific manner [ 51 ].…”

Genotypic Characterization of Epstein Barr Virus in Blood of Patients with Suspected Nasopharyngeal Carcinoma in Ghana

“…The follow-up study will associate virulent factors with the EBV genotypes, and possibly suggest a mechanistic role of the factors in disease etiology, which will ultimately drive the search for therapeutic targets. The classification of EBV into the two main geographically distinct genotypes, 1 and 2, is based on sequence polymorphism in EBNA-2, -3A, -3B and -3C [ 21 , 22 ]. However, since EBNA-2 has the least percentage of sequence homology EBV typing has been done using this protein [ 17 ].…”

Dysbiosis of Oral Microbiota and Its Effect on Epithelial-Mesenchymal Transition: a Review

“…E6 can associate with Bac-Bax and other pro-apoptotic proteins [118]. The onco-protein E6 can magnify cell proliferation without interference of E7 by means of its C-terminal PDZligand domain [119], as well as mediate suprabasal cell proliferation [120] which may lead to disruption of cell to cell adhesion and progression of carcinoma. Studies showed that the downregulation of E-cadherin increases the risk of metastasis in HNSCC [121].…”