Variations Among Isolates of Epstein‐Barr Virus* (original) (raw)
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Epstein-Barr virus associated diseases: an update
The Malaysian journal of pathology, 1993
The Epstein-Barr virus (EBV), traditionally linked etiologically with infectious mononucleosis (IM), endemic Burkitt lymphoma (BL) and nasopharyngeal carcinoma (NPC) has in recent years been associated with a host of other conditions. Viral strategies for entry into cells and persistence, as well as various molecular mechanisms involved in latency, replication and transformation have been elucidated. EBV termini analysis has demonstrated the essentially clonal nature of BL, NPC and preneoplastic lesions of the nasopharynx. Strain variation between isolates of EBV suggests that differences in epithelial cell tropism among strains may exist. Treatment of EBV-associated syndromes is largely supportive although antivirals may play a role in the management of oral hairy leukoplakia. At the present time, the development of an effective vaccine remains a viable proposition.
Histopathology, 1995
A study of the association of Epstein-Barr virus with Burkitt's lymphoma occurring in a Chinese population There is a strong association (approximately 95%) of endemic Burkitt's lymphoma with Epstein-Barr virus (EBV), whereas the association is weak for the sporadic form occurring in Western countries (approximately 15%). In the Middle East, North Africa and South America, 60-80% of Burkitt's lymphomas harbour EBV. These epidemiological differences suggest that either the endemicity of EBV or socioeconomic conditions, or both, may influence the pathogenetic role of EBV in Burkitt's lymphoma. Since only meagre data are available on Asians, this study was performed to address this issue by studying cases from Hong Kong, where EBV seroconversion occurs in the first few years of life but the socioeconomic conditions approach those of Western countries. In situ hybridization for EBV encoded RNAs (EBERs) was performed on paraffin sections of 18 cases of Burkitt's lymphoma. Labelling of the neoplastic cells was detected in five cases (2 7.7%). In contrast, among 54 cases of B-cell lymphomas of various subtypes studied for comparison, signals for EBER were detected in only one case each of T-cell-rich large B-cell lymphoma, anaplastic large cell lymphoma and Reed-Sternberg-like cells occurring in B-cell chronic lymphocytic leukaemia/small lymphocytic lymphoma. The strong labelling with oligo-dT probe (which hybridized with the polyadenylated ends of mRNA) in all cases suggested that the negative results were genuine and not due to poor preservation of RNA in the tissues. Thus, among B-cell neoplasms occurring in Chinese, Burkitt's lymphoma shows a statistically stronger association (P < 0.0 1) with EBV than with other types of B-cell lymphoma. The available data also suggest that the socioeconomic status of the country rather than exposure to EBV at an early age is the crucial factor determining the role of EBV in the genesis of Burkitt's lymphoma.
Epstein-Barr virus and cancers of the head and neck
American Journal of Otolaryngology, 2001
Denis Burkitt pioneered the association of viruses and cancer in humans with his observations of lymphomatous tumors in children in equatorial Africa. The Epstein-Barr virus (EBV), a human B lymphotrophic herpes virus, is strongly associated with undifferentiated carcinoma of the nasopharynx and African-type Burkitt's lymphoma. More recently, an association of this virus with other epithelial neoplasms, lymphomas, and immunodeficiencyrelated malignant and nonmalignant conditions has been reported. Since many of these tumors are rare, much of the information is based on sporadic reports and relatively small series of patients. The purpose of this report is to review the literature and examine the growing association of EBV with various head and neck malignancies.
Epstein-Barr Virus and Burkitt Lymphoma
The Lancet, 1978
In 1964, a new herpesvirus, Epstein-Barr virus (EBV), was discovered in cultured tumor cells derived from a Burkitt lymphoma (BL) biopsy taken from an African patient. This was a momentous event that reinvigorated research into viruses as a possible cause of human cancers. Subsequent studies demonstrated that EBV was a potent growth-transforming agent for primary B cells, and that all cases of BL carried characteristic chromosomal translocations resulting in constitutive activation of the c-MYC oncogene. These results hinted at simple oncogenic mechanisms that would make Burkitt lymphoma paradigmatic for cancers with viral etiology. In reality, the pathogenesis of this tumor is rather complicated with regard to both the contribution of the virus and the involvement of cellular oncogenes. Here, we review the current understanding of the roles of EBV and c-MYC in the pathogenesis of BL and the implications for new therapeutic strategies to treat this lymphoma.
Open Infectious Diseases Journal, 2010
Epstein-Barr virus (EBV) infection has been implicated in the aetiopathogenic mechanisms of several neoplastic and non-neoplastic disorders. Although the precise mechanisms of the tumourigenic actions of EBV have not yet been fully elucidated, this virus has been strongly linked to subtypes of Hodgkin's and non-Hodgkin's lymphomas (especially Burkitt's lymphoma), HIV/AIDS lymphomas, nasopharyngeal carcinoma and gastric carcinoma, among several others. The fact that persistent infections occur in greater than 95% of adults with an overall relatively low incidence of EBV related tumours compared with the prevalence of infection shows that there are definitely many other factors (genetic and environmental) that contribute to tumour development in EBV positive individuals. In this article, we review some of the currently available knowledge about these relationships in the commonly encountered EBV-associated malignancies. It is hoped that with continued research in the pathogenic mechanisms of EBV, specific roles will be identified that will facilitate the development of specific targeted therapy.
Epstein–Barr virus and carcinogenesis: beyond Burkitt's lymphoma
Clinical Microbiology and Infection, 2009
Subsequent to its discovery over 45 years ago, Epstein-Barr virus (EBV) has been associated with numerous human carcinomas. Approximately 95% of the world's population sustain an asymptomatic lifelong EBV infection. EBV persists in the memory B cell pool of normal healthy individuals and any disruption of this interaction results in virus-associated B cell tumours. The association of EBV with epithelial cell tumours, specifically nasopharyngeal carcinoma and EBV-positive gastric carcinoma, is less clear and is currently considered to be a consequence of the aberrant establishment of virus latency in epithelial cells displaying pre-malignant genetic changes. Although the precise role of EBV in the carcinogenic process is currently poorly understood, the presence of the virus in all tumour cells provides opportunities for the development of novel therapeutic and diagnostic approaches. The study of EBV and its role in carcinomas continues to provide insights into the carcinogenic process that are relevant to a broader understanding of tumour pathogenesis and to the development of targeted cancer therapies.
Oncotarget, 2016
The Epstein-Barr virus (EBV) is etiologically associated with the development of multiple types of tumors, but it is unclear whether this diversity is due to infection with different EBV strains. We report a comparative characterization of SNU719, GP202, and YCCEL1, three EBV strains that were isolated from gastric carcinomas, M81, a virus isolated in a nasopharyngeal carcinoma and several well-characterized laboratory type A strains. We found that B95-8, Akata and GP202 induced cell growth more efficiently than YCCEL1, SNU719 and M81 and this correlated positively with the expression levels of the viral BHRF1 miRNAs. In infected B cells, all strains except Akata and B95-8 induced lytic replication, a risk factor for carcinoma development, although less efficiently than M81. The panel of viruses induced tumors in immunocompromised mice with variable speed and efficacy that did not strictly mirror their in vitro characteristics, suggesting that additional parameters play an important role. We found that YCCEL1 and M81 infected primary epithelial cells, gastric carcinoma cells and gastric spheroids more efficiently than Akata or B95-8. Reciprocally, Akata and B95-8 had a stronger tropism for B cells than YCCEL1 or M81. These data suggest that different EBV strains will induce the development of lymphoid tumors with variable efficacy in immunocompromised patients and that there is a parallel between the cell tropism of the viral strains and the lineage of the tumors they induce. Thus, EBV strains can be endowed with properties that will influence their transforming abilities and the type of tumor they induce.