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Query: UMLS:C0001175 (AIDS)
 120,706 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with the acquired immunodeficiency syndrome (AIDS) acquire undifferentiated B-cell lymphomas that are similar to African Burkitt's lymphoma and contain Epstein-Barr virus (EBV). Using an in vitro assay system that measures a complex of cellular responses to EBV-infected lymphocytes, we found that B cells from 7 patients with AIDS and from 10 patients with AIDS-related disorders produced abnormally low numbers of immunoglobulin-secreting cells (P less than 0.001 as compared with normal controls) and that T-cell suppression, which was greater than 80 percent in EBV-seropositive normal controls, was absent. Instead, the patients' T cells markedly increased immunoglobulin production induced by EBV. In further studies, we determined that the mean frequency of circulating EBV-infected B cells capable of spontaneous outgrowth in vitro was 13 per 10(6) B cells in 7 patients with AIDS and 21 per 10(6) B cells in 10 patients with AIDS-related disorders--figures that were significantly higher than the mean in normal controls (P less than 0.001). Thus, patients with AIDS or AIDS-related disorders may be predisposed to the development of EBV-containing lymphomas, because they have a profound defect of T-cell immunity to EBV and abnormally high numbers of EBV-infected B cells in the circulation.
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PMID:Defective regulation of Epstein-Barr virus infection in patients with acquired immunodeficiency syndrome (AIDS) or AIDS-related disorders. 300 62

Aside from opportunistic infections, several neoplasms have been identified as part of the spectrum of acquired immunodeficiency syndrome (AIDS) as defined by the Centers for Disease Control. Kaposi's sarcoma (KS) was the first such neoplasm to be recognized within the spectrum of AIDS. Although the classic form of Kaposi's sarcoma had been well recognized prior to the epidemic of AIDS, it was quite distinct from the illness that was seen in its "epidemic" form in young homosexual males. In this setting, Kaposi's sarcoma is an aggressive disease, with extensive involvement of skin and mucous membranes, early dissemination to lymph nodes, impressive development of extreme lymphedema, even in the absence of bulky adenopathy, and rapid spread to visceral organs, including lungs and gastrointestinal tract, among others. Although rapid clinical progression and short median survival have been the rule, a spectrum of disease has been seen such that some patients have survived for many years with disease limited to the skin. Certain clinical and laboratory features, such as presence of unexplained fever, night sweats, weight loss ("B" symptoms), or significant T-4-lymphocytopenia, have been identified as indicators of poor prognosis. Various therapeutic interventions have been employed in epidemic KS, and although partial and complete remissions have occurred, no regimen yet reported has significantly improved the survival of treated patients. High-dose recombinant alpha interferon has produced response rates in approximately 30% of treated patients, although toxicity has been observed in approximately 30% as well. Likewise, vinblastine has produced similar response rates with no evidence of long-term efficacy or "cure." Aside from Kaposi's sarcoma, lymphoma primary to the central nervous system was recognized early in the AIDS epidemic as a criterion for inclusion within AIDS in patients less than sixty years of age. Several years after the initial reports of disease, it became apparent that specific types of systemic lymphoma were also quite extraordinary, and the definition of AIDS was amended in June 1985 to include high-grade B-cell lymphomas in individuals who had positive serology or virology for the human immunodeficiency virus (HIV). The AIDS-related lymphomas are characteristic, both pathologically and clinically. The vast majority of these cases have been high-grade B-lymphoid tumors of either immunoblastic or small-non-cleaved type (also known as "undifferentiated," Burkitt, or Burkitt-like).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Malignancies in the acquired immunodeficiency syndrome. 360 70

Kaposi's sarcoma and B-cell lymphomas have been reported to develop in homosexual men with the acquired immunodeficiency syndrome (AIDS) or chronic lymphadenopathy syndrome (CLS). We treated what we believe is the first documented case of multiple myeloma complicating CLS in a 31-year-old male homosexual. This broadens the spectrum of B-cell neoplasms associated with AIDS and has implications for the pathogenesis of B-cell lymphomas and the evaluation of these high-risk patients.
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PMID:Multiple myeloma in a homosexual man with chronic lymphadenopathy. 392 Sep 86

During one year, 55 bone marrow biopsies from 49 patients with CDC-defined acquired immune deficiency syndrome (AIDS) were studied. Eighty-three percent were normocellular or hypercellular; 17% were hypocellular. Marrow plasma cells were increased in 83% of patients, most showing polyclonal hypergammaglobulinemia. Forty percent of patients showed peripheral neutropenia, 29% thrombocytopenia, and 79% lymphopenia with markedly reduced T4+ lymphocytes. Eighty-five percent of patients were anemic, with iron studies showing a pattern consistent with the anemia of chronic disease. Mycobacterium avium-intracellulare (MAI) grew from ten (20%) biopsies, four with granuloma and six without granuloma (five of these six also showed marrow hypocellularity). Small poorly formed granuloma (70-150 micron) were seen in eight (16%) patients (four AFB-culture positive, 4 negative). Three of four granuloma-positive, culture-negative cases eventually grew MAI from autopsy material. Five (10%) patients had lymphoplasmacytic aggregates; later, one developed lymphoma, another, markedly atypical lymphoid hyperplasia. Two additional patients showed marrow B-cell lymphomas. Of these findings, only marrow MAI meets the CDC definition of AIDS. However, in this series, small ill-defined granulomas, lymphoplasmacytic aggregates, and B-cell lymphomas also were found. The authors conclude that these latter findings, when seen in high-risk patients, particularly those with lymphopenia, anemia, and/or hypergammaglobulinemia, also strongly suggest the diagnosis of AIDS.
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PMID:The bone marrow in AIDS. A histologic, hematologic, and microbiologic study. 403 75

The acquired immunodeficiency syndrome (AIDS) occurs in a subgroup of male homosexuals having sexual contact with a large number of partners. Uncommonly, AIDS has also been diagnosed in Haitians, hemophiliacs, and intravenous drug users and their infants. Manifestations include autoimmune disturbances, opportunistic infections, Kaposi's sarcoma, chronic lymphadenomegaly, non-Hodgkin's lymphoma, or squamous cell carcinoma. The hypothesis receiving most consideration is that a yet-to-be-identified virus causes AIDS. An alternative view is that repeated sexual involvement with multiple partners, in a subgroup of male homosexuals, exposes the men to the immunosuppressive impact of cytomegalovirus (CMV) and allogeneic semen. Antibody to asialo-Gm1 and other antigens on sperm react with and impair lymphoid cells. We propose a biphasic process. First, a reversible acquisition phase of impaired T-cell immunoregulation permits reactivation of Epstein-Barr virus (EBV), and autoantibodies are produced by the activated B cells. If sexual activity continues at a high level, accumulating immune defects, including destruction of thymic epithelium, lead to a second, self-sustaining phase wherein cytotoxic lymphocytes fail to eliminate herpesvirus-infected cells. Evidence is mounting that Kaposi's sarcoma is caused by CMV and that EBV is responsible for the B-cell lymphomas in these patients. Multiple factors, rather than a novel virus, probably induce AIDS in male homosexuals. If this hypothesis is correct, then rational bases for prevention and intervention can be designed.
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PMID:Acquired immunodeficiency syndrome, opportunistic infections, and malignancies in male homosexuals. A hypothesis of etiologic factors in pathogenesis. 630 Apr 80

The immune system is constantly challenged by ubiquitous viruses. Multiple immune defenses have evolved to meet these challenges, and thus immunocompetent individuals successfully respond to infection without sequela. X-linked lymphoproliferative syndrome patients, renal allograft recipients, and acquired immunodeficiency syndrome patients share impaired immune surveillance as a common feature. Such individuals are variously susceptible to numerous untoward complications following infection with Epstein-Barr virus, cytomegalovirus, herpes simplex virus, human papillomavirus, and hepatitis B virus. We hypothesize that failure of the immune system to control these viruses is instrumental in the occurrence of some B-cell lymphomas. Kaposi's sarcoma, and squamous-cell and hepatocellular carcinomas. Herein we review some mechanisms responsible for the breakdown of immune surveillance and the permissive role immunodeficiency plays in viral oncogenesis.
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PMID:Oncological consequences of impaired immune surveillance against ubiquitous viruses. 630 92

CD40 is expressed on both normal and neoplastic B lymphocytes. Signal transduction through CD40 in vitro has been shown to exert stimulatory effects on normal B cells and inhibitory effects on Epstein-Barr virus (EBV)-induced B-cell lymphoma lines and some other cell lines derived from patients with aggressive histology lymphoma. The transfer of normal human peripheral blood lymphocytes (huPBL) from EBV-seropositive donors into severe combined immune deficient (SCID) mice has been previously shown to result in the generation of human B-cell lymphomas. These tumors are similar to the highly aggressive EBV-induced lymphomas that can arise clinically after transplantation or in the setting of immunodeficiency. Treatment of huPBL-SCID chimeric mice with anti-CD40 or anti-CD20 monoclonal antibodies (MoAb) significantly delayed the development of EBV-induced B-cell lymphoma. However, the effects of the two MoAb were mechanistically distinct. Anti-CD40 treatment prevented lymphoma generation, while still allowing for functional human B-cell engraftment in the huPBL-SCID mice compared with mice receiving no treatment, all of which succumbed to lymphoma. By contrast, treatment with anti-CD20 significantly inhibited total human B-cell engraftment in the SCID recipients, which accounted for the absence of lymphomas. In vitro assays examining the transformation of human B cells by EBV also indicated that anti-CD40 could directly inhibit EBV-transformation, whereas anti-CD20 antibodies had no effect. Thus, anti-CD40 exerts selective effects to allow for the engraftment of normal human B cells and prevent the emergence of EBV lymphomas. Stimulation of CD40 by antibodies or its physiologic ligand may, therefore, be of significant clinical use in the prevention of EBV-induced B lymphomas that may arise when EBV-seropositive individuals receive immunosuppressive regimens after transplantation or in immune deficiency states, such as acquired immune deficiency syndrome.
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PMID:Antibodies to CD40 prevent Epstein-Barr virus-mediated human B-cell lymphomagenesis in severe combined immune deficient mice given human peripheral blood lymphocytes. 754 49

B-cell lymphomas developed frequently (approx. 40%) in SIVsm (SMM3) immunosuppressed monkeys and were mostly extranodal, aggressive and all associated with an EBV-related simian herpes virus operationally designated herpes virus Macaca fascicularis (HVMF-I). Lymphoma tissues from 21 monkeys were studied by PCR and DNA PAGE for mono/oligoclonality of the VDJ-rearranged IgH genes. Most lymphomas (n = 15) showed a monoclonal and approximately 1/3 (n = 6) an oligoclonal VDJ rearrangement pattern. The time after infection to tumor presentation was significantly shorter for oligoclonal than for monoclonal lymphomas, suggesting that oligoclonal selection frequently precedes the outgrowth of a single malignant clone. Comparison of the VDJ rearrangements in an established lymphoma cell line and the original, oligoclonal lymphoma tissue indicated in vitro selection of one HVMF-infected clone. Longitudinal studies of sequential lymph-node biopsies showed that the malignant lymphoma clone in 3 out of 8 lymphomas could be identified as a predominant clone in lymph nodes 2-12 months after SIV infection and 6-10 months before clinical presentation of the lymphomas. VDJ-rearranged DNA corresponding to that of the lymphomas was also detected in most sera at the time of lymphoma manifestation but not in corresponding PBL preparations. Clearly, the SIVsm AIDS model in cynomolgus monkeys represents a powerful tool for biological and clinical studies of herpes-virus-associated lymphomagenesis in immunosuppressed states.
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PMID:B-cell lymphomagenesis in SIV-immunosuppressed cynomolgus monkeys. 775 63

Mice inoculated with replication-competent stocks of the murine acquired immunodeficiency syndrome (MAIDS) virus are severely immunocompromised and proned to the development of T- and B-cell lymphomas. We have studied the development of T-cell lymphomas in C57BL/6 and RF/J mice inoculated with helper-free stocks of the MAIDS defective virus. We observed the expansion of T cell clones (detected by TCR gene rearrangements and by transplantation) only rarely in diseased C57BL/6 mice and slightly more frequently in RF/J mice. We succeeded in establishing four transplantable T cell tumors and malignant cell lines. The three cell lines from RF/J mice were immature T-cells (Thy-1+, CD3-, CD4+, CD8+, Mac-1+), while the line from the C57BL/6 mouse had the phenotype of mature T-cells (Thy-1+, CD3+, CD4+, CD8-). All lines were virus-producers despite the fact that helper-free stocks of the virus were inoculated. These helper MuLVs most likely originated from endogenous MuLV sequences. Also, the defective viral genome was clearly detectable in one cell line and was rearranged in two other lines. These established cell lines may be useful to determine whether they share some of the characteristics of the anergic T-cells in vivo and to study the role of the MAIDS defective virus in T cell transformation.
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PMID:Establishment of leukemic T-cell lines from mice inoculated with the MAIDS defective virus. 783 10

Non-Hodgkin's lymphomas have been recognized as an important and frequently fatal part of the spectrum of diseases associated with HIV infection. These are most often high-grade B-cell lymphomas usually of immunoblastic and small cell non-cleaved subtypes. Sporadic reports of T-cell lymphomas associated with HIV infection are found in the literature. Two have been reported to be CD30 positive presenting with lymph node and skin involvement. We report a case of an AIDS patient with a T-cell anaplastic large-cell lymphoma that was CD30-positive and presented in bone. This is most probably a sporadic event rather than another part of the AIDS-associated spectrum of disease.
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PMID:Anaplastic large-cell lymphoma presenting primarily in bone in a patient with AIDS. 798 53


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