They occur predominantly in males who have HIV/AIDS, had a solid organ transplant, or are immunosuppressed in other ways; ~5% of all individuals with PBL appear to be immunocompetent, i.e. to have no apparent defect in their immune system. The malignant plasmablasts in more than half the cases of PBL are infected with a potentially cancer-causing virus, Epstein–Barr virus (EBV), and rare cases of PBL appear due to the  plasmablastic transformation of a preexisting low-grade B-cell lymphoma. One variant of PBL, sometimes termed plasmablastic lymphoma of the elderly, has a significantly better prognosis than most other cases of PBL. The development of this variant appears due, at least in part, to immunosenescence, i.e. the immunodeficiency occurring in old age. Presentation
Plasmablastic lymphoma lesions are most commonly rapidly growing, soft tissue masses that may be ulcerating, bleeding, and/or painful. In a recent (2020) review of published cases, individuals presenting with PBD were typically middle-aged or elderly (range 1–88 years; median age 58 tears) males (~73% of cases). Only a few cases have been reported in pediatric cases. The PDL lesions occurred most commonly in lymph nodes (~23% of cases), the gastrointestinal tract (~18%), bone marrow (16%), and oral cavity (12%). Less frequently involved tissues include the skin, genitourinary tract, paranasal sinuses, lung, and bones.
Some of the gene abnormalities found in PBL 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). Diagnosis
Microscopic examination of involved PBD masses and infiltrates generally reveals diffuse proliferations of immunoblast-like cells with prominent features of plasma cells, i.e. plasmablastic cells. Immunostaining of these cells indicate that they lack B-cell marker proteins (e.g. CD20 and PAX5 [in ~10% of cases CD20 may be expressed at very low levels]) but rather express plasma cell marker proteins (e.g. CD38, CD138, IR4/MUM1, XBP1, IL21R, and/or PRDM1). The abnormalities in gene structures and expressions reported in the Pathophysiology section, particularly rearrangement and/or over expression of the MYC proto-oncogene, may also be apparent in these cells.