Epstein–Barr virus infection in cancer

EBV was the first human oncogenic virus identified. It was discovered in tumour cells isolated from Burkitt’s lymphoma tissue by Sir Anthony Epstein and Dr Yvonne Barr in 1964. Some years after its discovery, EBV was shown to be able to transform normal leukocytes into lymphoblastoid cell lines (LCLs). Since then, EBV has been found to be associated with many malignancies originating from lymphocytes or epithelial cells (Burkitt’s lymphoma, post-transplant and HIV-associated lymphomas, Hodgkin’s lymphoma, T-cell lymphoma, extra-nodal nasal-type natural killer/T-cell lymphoma, nasopharyngeal cancer, and a subset of gastric cancers), contributing to 1.5% of all cancer cases worldwide and approximately 200,000 new cases every year. However, this virus is found in more than 90% of healthy adults worldwide, indicating that EBV infection alone is not enough to cause cancer. The specific geographical distribution of some EBV-associated malignancies (such as Burkitt’s lymphoma in equatorial Africa and nasopharyngeal cancer in East Asia) indicates that the development of an EBV-associated neoplasm requires different environmental and genetic co-factors, of which only some are currently known. In this Special Issue, we present a collection of 26 papers (9 research papers and 17 reviews) covering a range of topics related to EBV infection in cancer patients. These fall into three general areas: (1) EBV-encoded genes; (2) EBV and immune responses; and (3) EBV-associated malignancies and EBV-targeted therapies. In this Special Issue, we aim to further elucidate the role of EBV infection in EBV-driven malignancies by reviewing the literature and reporting new findings addressing some of the unanswered questions in the field of EBV