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Epstein–Barr virus-infected B cells are human B lymphocytes that have been infected and transformed by Epstein–Barr virus (EBV). EBV efficiently infects and activates resting B lymphocytes, inducing their proliferation and transformation into immortalized lymphoblastoid cells. This process involves coordinated activation of host cell signaling pathways (e.g., STAT3, p38-MK2) and expression of key viral proteins (such as EBNA2 and LMP1) that drive oncogenic signaling, reprogramming the cell for viral latency and immune evasion[1][5][7]. EBV-infected B cells play central roles in various infectious, inflammatory, and neoplastic diseases, including infectious mononucleosis, Burkitt’s lymphoma, Hodgkin’s disease, and other EBV-driven B cell lymphomas[5][2]. However, unlike classical molecular targets (such as receptors or enzymes), this term denotes a cell population with altered molecular biology consequent to viral infection, rather than a discrete target suitable for direct molecular pharmacology.
Depletion of B cells (monoclonal antibodies like rituximab bind CD20, leading to killing of both infected and uninfected B cells)[5] Inhibition of viral replication (antivirals reduce EBV load, indirectly impacting infected B cells)
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