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Epstein-Barr virus latent antigens are a set of viral proteins and non-coding RNAs expressed during EBV's latent infection phase, primarily in B cells, enabling viral persistence as an episome without lytic replication. Key members include six EBNAs (EBNA1 for genome maintenance and transcription; EBNA2, EBNA-LP, EBNA3s for B-cell growth transformation via c-Myc upregulation and cell cycle modulation), three LMPs (LMP1 mimicking CD40 to activate NF-κB for survival; LMP2A/2B sustaining BCR-like signaling), abundant EBERs (promoting resistance to apoptosis via PKR inhibition and immune modulation), and BART miRNAs (targeting apoptosis regulators like BIM). These antigens drive three latency programs (I-III), with type III in immunodeficient states showing full expression for proliferation, type II in Hodgkin lymphoma and nasopharyngeal carcinoma featuring LMP1/LMP2, and type I in Burkitt lymphoma limited to EBNA1/EBERs/LMP2. In disease, they contribute to EBV-associated cancers (e.g., posttransplant lymphoproliferative disease, lymphomas) by reprogramming host cells for survival, proliferation, and immune escape, often via NF-κB, PI3K, and epigenetic changes. While no approved small-molecule drugs directly target them, EBNA1 is pursued for inhibition to disrupt persistence, and therapeutic antibodies are in development; EBER/LMP expression serves as diagnostic biomarkers in tumors[1][2][3][5][7][11].
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