Epstein‐Barr virus infection and human malignancies

Abstract

The Epstein-Barr virus (EBV) is a herpes virus which establishes a life-long persistent infection in over 90% of the human adult population world-wide. Based on its association with a variety of lymphoid and epithelial malignancies, EBV has been classified as a group 1 carcinogen by the International Agency for Research on Cancer. In this article we discuss the evidence supporting an aetiological role for EBV in the pathogenesis of human tumours. The biology of EBV infection will be described with special emphasis on viral transforming gene products. A brief survey of EBVassociated tumours is followed by a discussion of specific problems. Evidence is presented which suggests that failures of the EBV-specific immunity may play a role in the pathogenesis of EBV-associated tumours also in patients without clinically manifest immunodeficiencies. Finally, the timing of EBV infection in the pathogenesis of virus-associated malignancies is discussed. There is good evidence that EBV infection precedes expansion of the malignant cell populations in some virus-associated tumours. However, this is clearly not always the case and for some of these tumours there are indications that clonal genetic alterations may occur prior to EBV infection. Thus, whilst there is good evidence to suggest that EBV is a human carcinogen, its precise role(s) in the development of virus-associated human tumours requires clarification.

The oncogenic role of Epstein–Barr virus‐encoded microRNAs in Epstein–Barr virus‐associated gastric carcinoma

“…Constitutive activation of oncogene c-Myc is a key pathogenic factor in EBV-infected B cells, via chromosomal translocation, which has been considered as an interaction between EBV and c-Myc [70,71]. In addition, the finding of EBV terminal DNA repeats was also reported in up to 50% of cases of Hodgkin lymphoma [72,73]. However, the studies of EBV miRNAs in lymphoma are quite limited.…”

Hydroa vacciniforme‐like Epstein‐Barr virus‐associated monoclonal T‐lymphoproliferative disorder in a child

“…A clonal expansion of infected B or T cells may then progress to vari-ous lymphoproliferative disorders, such as Burkitt's lymphoma, Hodgkin lymphoma, lymphomatoid granulomatosis, nasal T or T/NK-cell lymphoma, NK-lymphoma/leukemia, angioimmunoblastic lymphadenopathy, and HV-like lymphoma. 7,21,25,26 Patients with chronic active EBV infection may also have intermittent fever, persistent hepatitis, hepatosplenomegaly, anemia, thrombocytopenia, interstitial pneumonitis, HV, and be hypersensitive to mosquito bites. 10,23,[27][28][29] Chronic active EBV infection behaves differently depending on whether it involves T cells or NK cells.…”

Stat3: linking inflammation to epithelial cancer - more than a "gut" feeling?

“…Chronic inflammation triggered by viral or bacterial infection increases the risk for the development of papilloma virus-associated cervical cancer [4,5], hepatitis B and C-associated hepatocellular carcinoma and Epstein Barr virus-associated lymphoproliferative disorder [6], and bacterial infections can promote metastasis following surgery [7]. In the gastrointestinal tract, Helicobacter pylori ( H.pylori )-associated gastric cancer along with ulcerative colitis and Crohn's disease-associated colorectal cancer comprise major health issues.…”