In addition to the immunodeficiency-causing viral disease, HIV/AIDS (which is an AIDS-defining clinical condition), recent studies have diagnosed<unk>  in individuals who have one or more other causes for immunodeficiency. These causes include prior organ transplantation; immunosuppressive drugs; autoimmune and chronic inflammatory diseases (e.g. hepatitis C, rheumatoid arthritis, Graves' disease, Giant-cell arteritis, sarcoidosis, and severe psoriasis); and immunosenescence due to age (e.g. >60 years). Rare cases of PDL have also occurred as a transformation of a low grade B-cell malignancy such as chronic lymphocytic leukemia/small lymphocytic lymphoma and follicular lymphoma. Studies also find that 60-75% of individuals diagnosed with<unk>  have Epstein-Barr virus-infected plasmablasts. EBV infects ~95% of the world's population to cause no symptoms, minor non-specific symptoms, or infectious mononucleosis. The virus then enters a latency phase in which infected individuals become lifetime asymptomatic carriers of the virus in a set of their B-cells. Some weeks, months, years, or decades thereafter, a very small fraction of these carriers, particularly those with an immunodeficiency, develop any one of various EBV-associated benign or malignant diseases, including, in extremely rare cases, Epstein–Barr virus-positive<unk> . The virus in infected<unk>  cells appears to be in its latency I phase; consequently, these infected cells express EBV products such as EBER nuclear RNAs and BART microRNAs. These RNAs promote infected cells to proliferate, avoid attack by the host's immune system's cytotoxic T-cells, and, possibly, block the infected cells' apoptosis (i.e. programmed cell death) response to injury The predisposing conditions described in the previous paragraph can serve to enhance the ability of the plasmablasts in<unk>  to: avoid the host's immune surveillance; survive for prolonged periods, grow excessively, and acquire pro-malignant gene abnormalities. Some of the gene abnormalities found in<unk>  include: 1) increased expression of the MYC proto-oncogene due to its rearrangement with an antibody gene by genetic recombination or, less commonly, other causes (Myc protein, the product of this gene, enhances cell proliferation, inhibits apoptosis, and promotes malignancy); 2) loss in the expression of the PRDM1 gene whose product, PRDM1/BLMP1 protein, represses the expression of Myc protein;) 3) frequent duplications in certain areas of chromosomes 1, 7, 11, and 22 (these duplications are similar to those often seen in diffuse large cell lymphoma); 4) reduced expression of at least 13 genes that are involved in B-cell responses to signaling agents. 5) increased expression of genes which promote the maturation of B-cells toward plasma cells (e.g. CD38, CD138, IR4/MUM1, XBP1, IL21R, and, as just indicated, PRDM1); and 6) reduced expression of genes characteristic of B-cells (e.g. CD20 and PAX5).
Plasmablastic lymphoma
Diffuse large B-cell lymphoma
Mixed-cell lymphoma
Marginal zone B-cell lymphoma
Aggressive lymphoma
Gray zone lymphoma
Follicular lymphoma
Anaplastic large-cell lymphoma