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

Herein we have provided a panorama of the clinical, histopathologic, and molecular biologic mechanisms of EBV-induced LPD particularly in immunosuppressed individuals. A listing of EBV-related diseases is shown in Table 4. We have stressed the frequent need to use multiple diagnostic methods for detecting EBV genome, particularly in immunodeficient patients who may fail to mount antibody responses to EBV. Given that we now recognize some of the immunocompromised patient populations at high risk for EBV-induced LPD, and have developed techniques for detecting EBV genome and early LPD, we may eventually prevent the occurrence of some of these life-threatening diseases. For example, we have learned to recognize and distinguish hepatic allograft rejection from EBV-induced LPD in hepatic biopsies (154). A periportal and sinusoidal infiltrate of small and large lymphoid cells, immunoblasts, and plasma cells, alert us to stain frozen liver sections for EBNA. Finding EBV guides the clinicians to reducing immunosuppression which then allows the restoration of immunosurveillance against the EBV-infected B cells. Whether an EBV vaccine can be successful in immunosuppressed individuals remains to be seen. As for other vaccines, many logistical problems prevail, such as the early occurrence of EBV infection during infancy in regions where BL is endemic. Surely, with the menacing threat that approximately 10% of patients with AIDS will develop NHL, new anti-viral therapy against EBV and the causative agent of AIDS and HIV, will be developed. The pathologist and virologist play essential roles in the recognition of EBV infection by performing clinical laboratory determinations. The characteristic histopathologic features of EBV-induced LPD are now recognized and when confirmed with molecular hybridization and immunofluorescent techniques will provide a solid diagnostic approach and, thus, a foundation for developing a sound therapeutic strategy.
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PMID:Epstein-Barr virus-associated lymphoproliferative disorders. 132 Jul 11

The data presented here indicate that the pathogenesis of AIDS-NHL is variably associated with multiple genetic alterations including monoclonal EBV infection, oncogene activation (c-myc, N-, Ki-ras) and tumor suppressor gene (p53) inactivation. Up to three (3 cases) or four (1 case) different lesions have been observed in the same tumor. The distribution of these lesions among the various histotypes is heterogeneous, although some preferential associations have been found either between lesion and histotype or between lesions. The most notable case involves p53 mutations/loss that is exclusively associated with the SNCC lymphoma subtype. Since alterations of the c-myc gene occur at very high frequency in this same histotype it is possible that both lesions may be required for the pathogenesis of the BL phenotype. The consistent negativity of p53 lesions in other NHLs associated or non associated with HIV infection (18) reinforces this hypothesis. Finally, we note that the frequency of p53 mutations is significantly higher in AIDS-BL than in non HIV-related BL (18), although the significancy of this difference remains to be assessed. This study confirms the relatively low frequency of EBV infection in systemic AIDS-NHL in general, but reinforces the notion that EBV may be required for the pathogenesis of AIDS-LC-IBP, as recently suggested by the high frequency of EBV positivity in primary CNS AIDS-NHL which are mostly represented by LC-IBP (2). Conversely, the low frequency of EBV sequences in the AIDS-SNCC lymphomas appears similar to that observed in sBL. Only in a small minority of cases were ras oncogene mutations found, mostly associated with the BL type.(ABSTRACT TRUNCATED AT 250 WORDS)
AIDS Res Hum Retroviruses 1992 May
PMID:Molecular pathogenesis of HIV-associated lymphomas. 132 69

Host susceptibility factors have been documented in both HD and NHL wherein a subset of pedigrees provide evidence for an autosomal dominantly inherited factor. Families with both HD and NHL occurring in genetically informative patients provide evidence in support of a possible common pathogenetic pathway for these diseases, as does recent cytogenetic and molecular genetic evidence. AIDS as an unmasking factor for familial predisposition to lymphoma and other cancers may be a powerful tool for identifying lymphoma- and cancer-prone families, but to date has not been employed. In concert with ecogenetic research, it will be important that lymphoma-prone families be subjected to multidisciplined research involving experimental designs developed by geneticists and epidemiologists in concert with pathologists, immunologists, and molecular geneticists.
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PMID:Genetics of Hodgkin's and non-Hodgkin's lymphoma: a review. 158 33

The association of malignant lymphoma with the acquired immunodeficiency syndrome (AIDS) has been recognized since early in the human immunodeficiency virus epidemic. Important clues regarding the etiology of AIDS-related non-Hodgkin's lymphoma (AIDS-NHL) and estimates of the future incidence of AIDS-NHL have been derived from epidemiologic studies. Recent epidemiologic and cohort studies reviewed in this article have confirmed that the incidence of non-Hodgkin's lymphoma is high in patients with human immunodeficiency virus infection, and increase with the duration of severe immunodeficiency in patients receiving antiretroviral therapies. A recent retrospective analysis of clinical features associated with AIDS-NHL described two groups of patients possessing distinct prognostic features. Finally, a number of new observations relating to the molecular and pathogenic mechanism underlying the development of AIDS-NHL have recently been described. The role of Epstein-Barr virus in the pathogenesis of AIDS-NHL continues to be enigmatic, and there may be multiple mechanisms contributing to the development of lymphoma, even in an individual patient.
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PMID:Clinical aspects of AIDS-related non-Hodgkin's lymphoma. 166 Nov 69

The AIDS-NHLs constitute a histologically diverse group of tumours. Comparisons with some groups of non-AID-NHLs, including eBL, sBL and large cell lymphoma, have been made and similar pathogenetic mechanisms postulated for such groups. However, the incidence of the different pathological types of NHL in AIDS is not yet clear, and further work is necessary to determine the contribution of factors such as c-myc translocations and the presence of EBV. AIDS-NHLs are clearly a more diverse group of tumours than their non-AIDS counterparts, and this probably reflects the involvement of a whole range of different pathogenetic stimuli that occur in individual AIDS cases.
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PMID:Aetiology and pathogenesis of non-Hodgkin lymphoma in AIDS. 166 31

Non-Hodgkin lymphoma developing in patients with HIV infection fulfills diagnostic criteria for AIDS. Clinical manifestations of AIDS-NHL are similar to those of malignant lymphoma arising in other acquired and congenital immunodeficiency states. AIDS related NHLs therefore consist primarily of tumours with B cell phenotype, intermediate or high grade histological subtype and rapid clinical progression with a high frequency of unusual extranodal involvement. Treatment of AIDS-NHL has been much less rewarding than treatment of lymphoma in non-HIV infected individuals. Complete response rates are lower than the corresponding rates seen in the non-HIV infected population, and responses that do occur tend to be of short duration. Improvements in treatment for AIDS-NHL will require the use of new therapies, designed to cause less myelosuppression, in conjunction with aggressive efforts to prevent opportunistic infections.
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PMID:Clinical manifestations and treatment of HIV related non-Hodgkin lymphoma. 182 18

The excess of NHL associated with HIV infection is well established. Clinically, HIV associated NHL is characterized by histological evidence of a high grade of malignancy, B cell origin, extensive extranodal involvement (most notably of the CNS) and poor prognosis. High grade B cell lymphoma or primary brain lymphoma in HIV infected individuals is considered diagnostic of AIDS by the Centers for Disease Control. The incidence of NHL among individuals with AIDS varies by subtype of lymphoma, age, sex, race and risk group. Younger individuals, males, whites and haemophiliacs are at higher risk than other groups. The incidence of HIV associated NHL is increasing. Because of the paucity of data on risk factors for this malignancy, the current possibilities for risk modification are limited to the prevention of HIV infection.
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PMID:Epidemiology of HIV associated non-Hodgkin lymphoma. 182 26

To investigate the range of pathology shown by acquired immune deficiency syndrome (AIDS)-related lymphomas arising in an epidemiologically well-defined group of patients, all cases of lymphoma recognized in Danish human immunodeficiency virus (HIV)-infected individuals up to the end of 1988 were studied. Twenty-seven cases (26 high-grade non-Hodgkin's lymphoma [NHL], 1 Hodgkin's disease) were found, to give a cumulative incidence rate of 8% among Danish AIDS patients. Morphologically most NHL patients were classified into two groups: 1) high-grade tumors with a predominant population of immunoblasts, either monomorphic or more often polymorphic with plasmacytic differentiation; 2) Burkitt-type. Of 26 NHLs, 22 had a B-cell paraffin-section immunophenotype and 4 were non-B, non-T. Epstein-Barr virus (EBV) DNA was demonstrated in tumor cells of 12 of 24 cases (50%) using in situ nucleic acid hybridization with a 35S-labeled probe in paraffin sections. Epstein-Barr virus DNA was found in 65% of group 1 and 20% of group 2 tumors. This study suggests the existence of two main groups of AIDS-related lymphoma with different pathogeneses. First there are immunoblast-rich lesions, which usually are associated with EBV and morphologically resemble lymphomas described in immunosuppressed organ-transplantation patients. Second there are Burkitt-type tumors in which EBV sequences are less common and that may be pathogenetically analogous to sporadic Burkitt's lymphoma.
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PMID:AIDS-related lymphoma. Histopathology, immunophenotype, and association with Epstein-Barr virus as demonstrated by in situ nucleic acid hybridization. 184 63

The Epstein-Barr virus (EBV) is associated with distinct forms of human lymphoid malignancies, including the endemic (eBL) and sporadic forms of Burkitt's lymphoma (sBL) and acquired immunodeficiency syndrome-associated non-Hodgkin lymphoma (AIDS-NHL). However, whether EBV has a pathogenetic role in these tumors or is a passenger virus has not been conclusively demonstrated. One element to distinguish between these two possibilities is to determine whether EBV infection has preceded and, thus, possibly contributed to clonal expansion, or whether infection has occurred after clonal expansion and thus is unlikely to contribute to pathogenesis. Toward this end we analyzed the structure of the heterogeneous genomic termini of EBV as markers of clonal infection in a panel of eBL (11 cases), sBL (9 cases), and AIDS-NHL (10 cases) biopsies. We show that EBV termini are uniformly clonal in sBL, eBL, and AIDS-NHL, strongly suggesting that EBV infection has preceded and, thus, most likely contributed to clonal expansion in these malignancies.
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PMID:Epstein-Barr virus infection precedes clonal expansion in Burkitt's and acquired immunodeficiency syndrome-associated lymphoma. 131 38

Recommendations regarding the current therapy of primary brain lymphoma (NHL-CNS) take into account the occurrence of this tumor in immunocompetent and immunosuppressed hosts. Immunohistochemical evaluation of biopsy material or spinal fluid provides the diagnosis in 90% of patients. For the immunocompetent, pre-irradiation intra-venous or intra-arterial chemotherapy with Methotrexate alone or in combination with other agents is provided to treat tumor within multiple brain sites. Subarachnoid deposits are treated with Methotrexate by intrathecal administration. Radiation is provided after chemotherapy and for the treatment of vitreal/retinal deposits or symptomatic lesions within the spinal axis. The therapy of recurrent NHL-CNS makes use of intravenous Methotrexate or high dose Cytosine Arabinoside. Immunosuppressed patients respond to reduction of immunosuppressive medication. The therapy of NHL-CNS in the AIDS patient makes use of corticosteroids followed by cranial irradiation. A discussion of emerging trends in the therapy of NHL-CNS in the AIDS and non-AIDS population is provided.
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PMID:The therapy of primary brain lymphoma. 189 64


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