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Query: UMLS:C1396851 (Epstein)
 24,119 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The polymerase chain reaction (PCR) technique was used to detect the presence of Epstein-Barr virus (EBV) DNA sequences in Hodgkin's disease specimens from 10 patients who were also positive for the human immunodeficiency virus (HIV). Eight of 10 specimens were positive for EBV, compared to 23 of 57 Hodgkin's disease specimens from patients without HIV infection, suggesting a closer association between Epstein-Barr virus infection and Hodgkin's disease in patients with HIV infection than in the general population.
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PMID:Epstein-Barr virus in Hodgkin's disease from patients with human immunodeficiency virus infection. 131 40

Since the original description of oral hairy leukoplakia among homosexual men in San Francisco in 1984, this white lesion of the tongue has been seen in the mouths of persons infected with the human immunodeficiency virus (HIV) worldwide. Its presence in HIV-positive persons usually but not always indicates fairly rapid progression to acquired immunodeficiency syndrome in the absence of antiretroviral therapy. Although the lesion appears to be common in HIV-positive persons, it is also, albeit rarely, seen in other conditions associated with immunosuppression. Epstein-Barr virus is associated with and presumably causes hairy leukoplakia, and the lesion offers insights into the biology of this ubiquitous DNA-oncogenic virus.
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PMID:Significance of oral hairy leukoplakia. 131 89

The identification of adenovirus in tissue can be difficult. In situ hybridization for adenovirus nucleic acids may aid in the demonstration of adenovirus infections. To develop a probe against adenovirus, a 978 bp fragment of DNA containing the VA-I, VA-II, and a portion of the L-1 regions of the adenovirus type 2 genome was cloned into the SK+ vector. These regions were selected because they are generally conserved among adenoviruses and are abundantly transcribed during the lytic cycle. Sense and antisense tritium or Digoxigenin-labeled riboprobes were generated using in vitro transcription and applied to formalin-fixed paraffin-embedded sections of HeLa cells infected with adenovirus type 2. Extensive in situ hybridization of the antisense riboprobe to HeLa cells with cytopathic changes was found. The number of cells to which the probe hybridized decreased proportionately with dilution of infected with noninfected cells. The control sense riboprobe showed only scattered breakthrough hybridization and in these cells hybridization was mainly located in the nucleus. Northern blot analysis of RNA from infected HeLa cells confirmed the in situ hybridization results. No hybridization was detected when cultured cells infected with herpes simplex virus, Epstein-Barr virus, cytomegalovirus, or human immunodeficiency virus were examined. Specific hybridization was detected in tissues obtained at autopsy from four patients with culture proven adenovirus infection. These observations suggest that this probe is useful in the diagnosis of adenovirus in formalin-fixed paraffin-embedded material.
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PMID:Virus-associated RNAs (VA-I and VA-II). An efficient target for the detection of adenovirus infections by in situ hybridization. 131 30

VAHS (virus associated hemophagocytic syndrome) is a severe clinical and biological condition associated with certain menacing viral infections. It has been observed in patients with manifest immunodeficiency but also in previously apparently healthy children. Epstein-Barr virus (EBV) infection, although it is sometimes unrecognized and insidious, is one of the etiologies to be considered. Differential diagnosis with other causes of macrophage activation is a delicate task in pediatrics. Better understanding of the pathophysiology of the syndrome offers interesting therapeutic prospects.
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PMID:[Histiocyte activation syndrome associated with EBV in children]. 131 25

Lymphocytic interstitial pneumonitis (LIP) and nonspecific interstitial pneumonitis (NIP) are pulmonary complications of human immunodeficiency virus (HIV) infection that occur in the absence of a detectable opportunistic infection or neoplasm. We reviewed lung biopsy specimens from 50 adult HIV-infected patients, of whom four had LIP and 46 had NIP. The majority (47 of 50) of specimens from patients with NIP showed mild chronic interstitial pneumonitis (CIP/NIP), with three showing features of diffuse alveolar damage, organizing phase. In contrast to CIP/NIP, the five specimens from four patients with LIP demonstrated more extensive lymphocytic interstitial infiltrates that extended into the alveolar septal interstitium. The majority of the interstitial lymphocytes in both NIP and LIP were of T-cell origin and stained for UCHL-1. The etiologies of NIP and LIP remain unknown. Since the common opportunistic infections were excluded by routine methods, we sought, with special techniques, to investigate whether HIV, Epstein-Barr virus (EBV), or cytomegalovirus (CMV) could be identified in lung biopsy specimens from these patients. By in situ hybridization, we found one LIP specimen with expression of large amounts of HIV RNA primarily within macrophages in germinal centers; in the remaining specimens, occasional cells expressing HIV RNA were found (two LIP and four NIP). Neither CMV nor EBV was found by in situ hybridization in seven specimens; in these same specimens EBV was detected using the polymerase chain reaction in only one case of NIP, similar to results in control specimens. These results, together with the knowledge that lymphocytic pulmonary lesions may be caused by lentiviruses in humans and animals, suggest that HIV plays a significant role in the pathogenesis of both NIP and LIP in adult HIV-infected patients; in contrast, our data do not demonstrate a direct role for either EBV or CMV.
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PMID:Lymphoid pneumonitis in 50 adult patients infected with the human immunodeficiency virus: lymphocytic interstitial pneumonitis versus nonspecific interstitial pneumonitis. 131 78

A 24 year old male with a history of eczema, recurrent mild infections, and thrombocytopenia consistent with the Wiskott-Aldrich syndrome (WAS) presented with a mediastinal mass, generalized lymphadenopathy, splenomegaly, and severe thrombocytopenia. Studies of immune function including immunoglobulin levels and T-cell subsets were normal. Furthermore, his T lymphocytes proliferated normally in response to phytohemagglutinin, concanavalin A, and the combination of neuraminidase/galactose oxidase. However, their proliferative responses to anti-CD43 antibody and periodate were diminished, consistent with the clinical diagnosis of WAS. An initial inguinal lymph node biopsy surprisingly revealed Kaposi sarcoma. However, following splenectomy to increase the platelet count, biopsy of the mediastinal mass revealed T-cell large cell lymphoma. Studies of biopsied tissue for the presence of Epstein-Barr virus and cytomegalovirus were negative, as were studies of blood, including the polymerase chain reaction, for the presence of the human immunodeficiency virus (HIV). This is the first report of Kaposi sarcoma arising in a patient with a congenital immunodeficiency syndrome. Although Kaposi sarcoma can arise in the face of the severe immunosuppression that follows allograft transplantation and in patients infected with HIV, we postulate that longevity in the face of mild immunosuppression was the major factor in the development of Kaposi sarcoma in this patient.
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PMID:Coincident Kaposi sarcoma and T-cell lymphoma in a patient with the Wiskott-Aldrich syndrome. 131 18

Taking advantage of the abundant expression of the small Epstein-Barr virus (EBV)-encoded RNAs (EBERs) in latently infected cells, we have analyzed 72 normal and hyperplastic lymph nodes and three tonsils of acute infectious mononucleosis (IM) for the presence and distribution of EBV+ cells using EBER-specific in situ hybridization, in some cases combined with immunohistologic demonstration of cell type-characteristic antigens. In IM, large numbers of EBV+ lymphoid B blasts were detectable in extrafollicular areas, whereas germinal centers were generally free of EBV+ cells. In reactive lymph nodes, the frequency of EBV+ cells varied with the degree of lymphoid hyperplasia and underlying immune status. The lowest numbers of EBV+ cells were detected in nonactivated lymph nodes and highest in human immunodeficiency virus-associated lymphadenopathy. If present in these lymph nodes, EBV+ cells were almost exclusively localized to extrafollicular areas, as also observed in IM. However, in contrast to IM, these cells were mainly small lymphocytes. Furthermore, in some instances, occasional scattered EBV+ cells were seen within germinal centers, and in two cases diffuse expansions of EBV+ cells occurred within a single germinal center each, indicating that under certain circumstances EBV+ B lymphocytes may participate in physiologic germinal center reactions. These findings reflect the interference of EBV with physiologic lymphoid differentiation pathways and provide a link to EBV-associated malignant lymphomas with a postulated origin from germinal center cells.
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PMID:Patterns of Epstein-Barr virus infection in non-neoplastic lymphoid tissue. 131 83

Excesses of non-Hodgkin's lymphoma have been observed among farmers exposed to phenoxyacetic acid herbicides and, less persuasively, among workers exposed to insecticides. Exposure to organic solvents (particularly chlorinated hydrocarbons) has also been associated with an increased risk of NHL. TCDD (which is a contaminant of phenoxy herbicides), DDT, and chlorinated solvents have all been reported to induce impairment or suppression of cell-mediated immunity. We hypothesize that NHL is caused by common viruses, such as the Epstein-Barr virus, that induce proliferation and immortalization of B-cells, followed by T-cell impairment entailing cell-mediated immunodeficiency. The increased risk of NHL with HIV infection and heart or kidney transplantation, in which immunodeficiency also occurs, is consistent with this hypothesis.
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PMID:The role of occupational exposure and immunodeficiency in B-cell malignancies. Working Group on the Epidemiology of Hematolymphopoietic Malignancies in Italy. 131 21

We have established a line of malignantly transformed human B cells by infecting purified primary B lymphocytes with human immunodeficiency virus type 1 (HIV-1). This line, termed B-HIV1, may serve as a model system for a subset of AIDS-related B-cell lymphomas in which the transformed phenotype may be initiated and/or maintained through an HIV-1 gene product. The B-HIV1 line contains both Epstein-Barr virus (EBV) and HIV-1 genomes. In addition, the c-myc gene is expressed at levels 10 to 20 times those in normal B cells. Similarly, EBV sequences, including those for the latent membrane protein (LMP), are expressed at greatly enhanced levels relative to expression in normal, EBV-immortalized B cells. The upregulation of c-myc and of EBV gene expression can both be produced by infection of susceptible B cells (not already harboring HIV) with exogenous HIV-1. The B-HIV1 line exhibits properties of malignantly transformed cells, in that it grows logarithmically in 1% serum, clones in soft agar, and produces invasive, malignant B-cell lymphomas in severe combined immunodeficient (SCID) mice. We have shown that HIV-1 has the ability to infect primary human B cells and to activate expression of EBV and c-myc. HIV activation of EBV has been documented previously in certain cell lines, here we note that such activation can occur in primary B cells and, under certain conditions, can result in outgrowth of immortalized cell lines. This phenomenon may contribute to the clinical manifestation of lymphadenopathy early after infection with HIV. In addition, we have demonstrated that HIV infection of primary B cells in vitro can result in appearance of a fully malignant phenotype. This phenotype is likely to be due, at least in part, to the activation of c-myc by HIV. Preliminary experiments indicate that Tat, the gene product of the transactivator of viral gene transcription tat, can upregulate c-myc transcription after addition to the culture media of certain B-cell lines. This raises the possibility that Tat can bind to target sequences in cellular RNA and enhance transcription as it does for HIV.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Human immunodeficiency virus activates c-myc and Epstein-Barr virus in human B lymphocytes. 131 11

The Epstein-Barr virus (EBV) has been classically associated with nasopharyngeal carcinoma and Burkitt's lymphoma, a monoclonal B-cell non-Hodgkin's lymphoma. Since the EBV genome has also been found in post-transplant lymphomas and lymphomas arising in individuals infected with the human immunodeficiency virus, evidence has now accumulated that EBV might be the initiator of a multi-step process leading from polyclonal B-cell hyperplasias to monoclonal lymphoma. In a retrospective study of 60 T-cell lymphomas of various types, we found EBV DNA in 21 (35%) using Southern- and/or dot-blot techniques. Eight of 14 nodal samples of angio-immunoblastic lymphadenopathy (57%) were shown to harbour detectable EBV DNA. The tumour with the next highest frequency, 47% (7/15 cases analyzed) was pleomorphic T-cell lymphoma, medium- and large-cell type; EBV was found both in nodal and in extranodal lymphomas of this type. Lymphoepitheloid (Lennert's) lymphoma and large-cell anaplastic lymphoma were positive in 2/5 and 3/8, respectively, of the cases analyzed. No viral DNA could be demonstrated in 3 T-immunoblastic and 5 T-lymphoblastic lymphomas. Clonotypic analysis revealed monoclonal as well as oligoclonal virus populations. Our data suggest that, at least in some of these entities, the presence of the EBV genome might be due to secondary mechanisms such as escape from immune surveillance.
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PMID:Prevalence of Epstein-Barr virus DNA in different T-cell lymphoma entities in a European population. 131 68


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