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Almost everyone carries Epstein-Barr virus for life without harm. Which lymphoma it can help cause depends on how many of its genes the infected cell is switching on, and that depends on how closely the immune system is watching.
Epstein-Barr virus was found by electron microscopy of cells cultured from Burkitt lymphoma, a childhood tumour whose distribution across equatorial Africa matched that of holoendemic malaria and so suggested a viral cause. It then turned out to be everywhere, persisting for life as an asymptomatic infection of the B-cell pool in the great majority of people (Young and Rickinson 2004). What makes it dangerous in a few of them is not the virus being present but which of its genes are switched on.
Latency I expresses only EBNA1, enough to keep the viral episome copied when the cell divides and almost nothing for a T cell to recognise. This is the Burkitt pattern, where the virus sits alongside a MYC translocation.
Latency II adds LMP1 and LMP2. LMP1 behaves like a CD40 receptor that is permanently switched on and drives NF-kB. This is the pattern in classical Hodgkin lymphoma and in extranodal NK/T-cell lymphoma.
Latency III expresses the full set of nuclear antigens and membrane proteins and will immortalise a resting B cell outright. It is kept in check entirely by T cells, which is why it appears when T cells are removed: post-transplant lymphoproliferative disorder, HIV-associated lymphoma, and EBV-positive large B-cell lymphoma in older people whose immunity has aged.
The practical consequences are few but real. Reducing immunosuppression is the first treatment of post-transplant lymphoproliferative disorder, and it is the one place where acting on the virus changes the plan. Plasma EBV DNA is used to follow response in NK/T-cell lymphoma and in post-transplant disease. EBV-specific T cells are licensed for post-transplant disease that has failed other treatment. The share of each lymphoma that is EBV-positive varies so widely by subtype, geography and age that this entry does not quote one.
In plain words · CD30 is a protein on the malignant Reed-Sternberg cells of Hodgkin lymphoma and on some T-cell lymphomas, and the address for the ADC brentuximab vedotin.
Showing the target this term concerns: CD30.
Shares HTLV-1, Tax and HBZ in adult T-cell leukaemia/lymphoma, Oncogenic viruses, Inflammation & NF-κB, Peripheral T-cell lymphomas (including cutaneous T-cell lymphoma).
Shares HTLV-1, Tax and HBZ in adult T-cell leukaemia/lymphoma, Oncogenic viruses, Inflammation & NF-κB, Peripheral T-cell lymphomas (including cutaneous T-cell lymphoma).
Shares HTLV-1, Tax and HBZ in adult T-cell leukaemia/lymphoma, Oncogenic viruses, Inflammation & NF-κB, Peripheral T-cell lymphomas (including cutaneous T-cell lymphoma).
Shares The Hodgkin microenvironment: when the cancer cell is the minority, CD30, Peripheral T-cell lymphomas (including cutaneous T-cell lymphoma), Hodgkin lymphoma.
Shares HTLV-1, Tax and HBZ in adult T-cell leukaemia/lymphoma, Oncogenic viruses, Inflammation & NF-κB, Peripheral T-cell lymphomas (including cutaneous T-cell lymphoma).
Shares HTLV-1, Tax and HBZ in adult T-cell leukaemia/lymphoma, Oncogenic viruses, Inflammation & NF-κB, Peripheral T-cell lymphomas (including cutaneous T-cell lymphoma).
Shares Plasma EBV DNA, Burkitt lymphoma, Peripheral T-cell lymphomas (including cutaneous T-cell lymphoma), Hodgkin lymphoma.
Shares Burkitt lymphoma, Peripheral T-cell lymphomas (including cutaneous T-cell lymphoma), Hodgkin lymphoma, Non-Hodgkin lymphoma (all types).