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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In recent years, techniques, probes, and reagents became available to reliably visualize individual Epstein-Barr virus (EBV)-infected cells, to assess EBV gene expression, and to analyze the clonal composition of EBV genomes in human tissues. Application of these techniques to more than 1000 lymphoid tissue specimens revealed (1) characteristic cellular and compartmental distribution patterns of EBV-infected cells in normal lymph nodes, reflecting the interference of EBV with physiologic B cell differentiation pathways, (2) an association of EBV with various mono- and oligoclonal lymphoproliferations ranging from benign conditions to overtly malignant lymphomas, and (3) characteristic patterns of EBV gene expression among EBV-associated lymphoproliferations. In the context of the established immortalizing and transforming properties of EBV, the findings support the concept of an etiologic role of EBV for cases of certain lymphomas such as Burkitt's lymphoma, anaplastic large cell lymphoma, Hodgkin's disease, and lymphomas arising in immunocompromised individuals. In contrast, lymphomas harboring EBV in only proportions of the tumor cells (such as cases of peripheral T cell lymphoma and some B cell lymphoma types) argue against an etiologic role in the primary process of malignant transformation for the virus in these instances. Since in many of these cases a proportion of the EBV infected tumor cells express the EBV oncoprotein LMP (latent membrane protein) the virus may influence, however, the proliferative properties as well as the morphological and molecular phenotype of the neoplastic cells.
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PMID:[Epstein-Barr virus associated lymphocyte proliferation]. 128 80

Distribution and phenotype of Epstein-Barr virus (EBV)-harboring cells were determined in Hodgkin's disease (HD) biopsies by in situ hybridization with [35S]-labeled RNA probes specific for the small EBV-encoded nuclear RNAs, EBER1 and EBER2, in some instances preceded by immunohistology for CD20, CD30, CD45RO, and CD68 antigens, the T-cell receptor beta-chain, and latent membrane antigen (LMP) of EBV. Twenty-three of 46 HD cases displayed EBER transcripts in all Hodgkin and Reed-Sternberg (H-RS) cells, and 18 of these cases showed LMP expression exclusively in neoplastic cells. EBER+ small reactive cells were present in 39 cases in low numbers, and in three cases in abundance. Thus, presence of H-RS cells with or without LMP expression was not accompanied by an unrestricted proliferation of reactive EBER+/LMP- lymphoid cells in the majority of HD patients. Simultaneous in situ hybridization with [35S]-labeled immunoglobulin light chain (IgLC) gene probes and nonisotopically labeled EBER probe showed a phenotype of mature B lymphocytes and a polyclonal composition for a large proportion of the EBER+ small cells. However, in contrast to noninfected cells, CD20 expression was not detectable in many of these cells, which may indicate downregulation of certain differentiation antigens in latently EBV-infected small lymphoid cells in vivo.
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PMID:Distribution and phenotype of Epstein-Barr virus-harboring cells in Hodgkin's disease. 132 Sep 54

A series of 33 cases of Hodgkin's disease was investigated for the presence of the EBV encoded latent gene product LMP-1 and of CD23 using immunohistochemical techniques. The expression of bcl-2 was examined in a subset of cases. LMP-1 was detected in the Reed-Sternberg cells in 15 cases. Although LMP-1 is known to upregulate CD23 and bcl-2, there was no correlation between the expression of LMP-1 and the detection of CD23 and bcl-2 in Reed-Sternberg cells.
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PMID:The expression of the EBV latent membrane protein (LMP-1) is independent of CD23 and bcl-2 in Reed-Sternberg cells in Hodgkin's disease. 132 89

Recombinant baculoviruses containing the complete LMP and truncated LMP genes were generated and high levels of the LMP proteins were expressed in Spadoptera Frugiperda insect cells. A specific rabbit antiserum directed against the N-terminal part of LMP was obtained by immunizing the rabbits with Escherichia coli-expressed trpE-N-terminal part of LMP fusion protein. A total of 127 human sera were studied for their immune response to the recombinant full-length LMP. In immunofluorescence analysis, all sera tested showed no detectable reaction with the recombinant full-length LMP. In immunoprecipitation-immunoblotting analysis, however, sera from patients with nasopharyngeal carcinoma (5/22), patients with Hodgkin's disease (16/27), patients with other diseases exhibiting high EA-IgG titers (3/52), and VCA-IgG-positive healthy individuals (2/26) were shown to contain antibodies against this recombinant LMP. The expressed LMP proteins provided a sufficient and economic source of the proteins for further serological and biological studies.
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PMID:Expression of the Epstein-Barr virus latent membrane protein (LMP) in insect cells and detection of antibodies in human sera against this protein. 132 1

Epstein-Barr virus (EBV) is believed to be implicated in the aetiology of non-Hodgkin's lymphomas developing in immunodeficient individuals including AIDS patients. EBV has also been associated with Hodgkin's disease (HD), where the genomes have been demonstrated in the Hodgkin and Reed-Sternberg cells in some of the cases. Recent evidence has shown that EBV genomes are transcribed in these cells, because the EBV-encoded latent membrane protein-1 (LMP-1) can be demonstrated in the tumour cells in about half of the HD cases in HIV-negative patients using immunohistochemistry. LMP-1 is of special interest as a possible oncogenic agent because of its strong transforming capacity in vitro. In this study we have examined the expression of LMP-1 in HD of HIV-positive patients compared with HD in HIV-negative patients. We investigated 18 lymph nodes from 16 HIV-positive patients with HD (eight mixed cellularity, nine nodular sclerosis, one unclassified) using the CS.1-4 anti-LMP-1 monoclonal antibodies, which can usually be applied successfully to archival biopsy material. In each case, 50-90 per cent of the tumour cells were labelled. Staining was excellent for both fixatives used (4 per cent buffered formalin, Bouin's fluid). It is concluded that EBV-encoded LMP-1 is firmly associated with HD of HIV-positive patients. This is most conspicuous in the nodular sclerosing subtype HD in HIV-positive patients, in which 100 per cent were LMP-1 positive as compared with 32 per cent of nodular sclerosis HD in HIV-negative cases in a previously published series. This difference is statistically significant (P < 0.001). The possible biological and clinical significance of this difference should therefore be studied in larger series.
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PMID:Frequent expression of Epstein-Barr virus latent membrane protein-1 in tumour cells of Hodgkin's disease in HIV-positive patients. 132 76

Epstein-Barr virus, a lymphotropic herpesvirus of humans, has potent B cell growth transforming activity yet persists in the lymphoid tissues of most individuals as a lifelong asymptomatic infection. Virus induced B cell growth transformation in vitro is associated with the expression of a limited set of viral genes encoding six nuclear antigens (EBNA 1, 2, 3A, 3B, 3C and LP) and two latent membrane proteins (LMP 1, 2). Healthy virus carriers possess strong EBV specific CTL memory that can be reactivated in vitro. Here, we summarize experiments in which the antigenic specificities of these HLA class I restricted memory CTL responses have been mapped in a range of individuals with different HLA backgrounds. Of the known EBV latent proteins, EBNA 3A, 3B and 3C are frequently the dominant targets for such responses, but examples of responses directed against epitopes of EBNA 2, EBNA-LP or the LMP have been identified; by contrast, CTL responses against epitopes of EBNA 1 have not been observed. Epstein-Barr virus is associated with at least three malignancies of lymphoid origin--immunoblastic lymphomas of the immunosuppressed, endemic Burkitt's lymphoma and a subset of Hodgkin's disease. The immunoblastic lymphomas express the complete spectrum of EBV coded latent proteins and a cellular phenotype similar to that of in vitro transformed B lymphoblastoid cell lines; accordingly, they remain sensitive to EBV specific CTL recognition. Endemic BL cells are not recognized by such CTL, and at least three consistent features of this tumour could contribute to immune escape: (a) allele specific downregulation of HLA class I antigen expression, (b) absence/low expression of cellular adhesion molecules and (c) restriction of EBV latent protein expression to EBNA 1 only. The relative importance of these three features of the BL cell phenotype with regard to sensitivity to CTL recognition is re-interpreted in the light of recent results. Finally, the pattern of virus latent protein expression in EBV positive Hodgkin's disease is described, and the possibility of EBV specific CTL control against this tumour is discussed.
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PMID:T cell recognition of Epstein-Barr virus associated lymphomas. 133 Mar

Epstein-Barr virus is associated with many diseases. Today, the pathologist may study either by immunohistochemistry or in situ hybridization on tissue sections: EBV genome, EBV messenger RNA, EBV latent and replicative proteins. Several technics can be performed on fixed paraffin-embedded tissue to demonstrate the presence of EBV DNA, EBER-1 RNA, LMP-1 protein. Frozen tissues are required for the study of EBNA-2, ZEBRA and replicating proteins expression. The results, obtained during the study of benign and malignant proliferations always or often associated with EBV, such as infectious mononucleosis, Burkitt's lymphomas, AIDS associated lymphomas, lymphoproliferations in immunocompromised patients, Hodgkin's disease, and some epithelial proliferations, are summarized.
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PMID:[Contribution of immunohistochemistry and in situ hybridization techniques in diseases caused by or associated with Epstein-Barr virus]. 133 77

The etiology of Hodgkin's disease (HD) is unknown, but a growing body of evidence suggests that the Epstein-Barr virus (EBV) plays a role in a proportion of cases. Clonal EBV genomes have been detected in affected tissues, and EBV has been localized to Reed-Sternberg (RS) cells, the putative malignant cells in HD. EBV latent genes, including the EBER RNAs and the latent membrane protein, LMP-1, are expressed by RS cells. These data suggest that EBV is playing a role in the pathogenesis of HD; however, it is clearly not involved in all cases. Using in situ hybridization, we can detect EBV within the RS cells in approximately 40% of cases. Epidemiological data suggest that HD is a heterogeneous condition and the distribution of EBV-associated cases is not random. Studies from several groups indicate that mixed cellularity cases are more likely to be EBV-associated than nodular sclerosis cases. Our data further suggest that the majority of pediatric and older cases of HD are EBV-associated, whereas the RS cells in young adult cases only rarely harbor EBV. We therefore speculate that another virus is responsible for the young adult peak in incidence which is seen in developed countries.
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PMID:Viral involvement in Hodgkin's disease. 133 12

In Hodgkin's disease, Epstein-Barr virus (EBV) is found in CD30-positive Reed-Sternberg cells. We therefore studied 60 CD30-positive non-Hodgkin's lymphomas (NHLs) for the presence of EBV by the polymerase chain reaction (PCR) and DNA in situ hybridization (DISH), and by immunohistochemistry for the latent EBV proteins LMP and EBNA-2. CD30-negative NHLs and reactive lymph nodes served as controls. The CD30-positive cases comprised 17 anaplastic large cell lymphomas (ALCLs) (> 75 per cent CD30-positive cells) and 43 non-ALCLs (with 5-35 per cent CD30-positive cells). By PCR, 40 of 60 CD30-positive NHLs (67 per cent) were EBV-positive; in CD30-negative cases, 6/29 (21 per cent) were EBV-positive, as were 12/50 (24 per cent) reactive lymph nodes. The DISH procedure demonstrated the EBV genome exclusively in the nuclei of tumour cells in 23 of the 37 PCR EBV-positive cases that were tested. PCR-negative cases were always DISH-negative, as were the PCR-positive reactive lymph nodes and CD30-negative NHLs. Immunohistochemistry demonstrated LMP in neoplastic cells of 7/47 (15 per cent) CD30-positive NHLs, both ALCL and non-ALCL always in PCR EBV-positive cases, but never in the two control groups. EBNA-2 staining could not be detected. It is concluded that EBV is present (and transcriptionally active) in a sizeable number of NHLs and an association between the presence of the EBV genome and CD30 expression seems likely.
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PMID:High incidence of EBV genome in CD30-positive non-Hodgkin's lymphomas. 133 46

Epstein-Barr virus (EBV) DNA is frequently identified in benign and malignant lymphoproliferative conditions. As shown by in situ hybridization studies viral DNA is localized within malignant cells as well as benign lymphocytes. Clonal and nonclonal EBV genomes are present in Hodgkin's disease (HD), lymphomas of the immunocompromised host and reactive lymph node hyperplasia. Lytic infection with formation of linear genomes is observed in the same conditions but appears to be infrequent in HD as shown by quantitation of mRNA coding for viral capsid antigen. Expression of the oncogene LMP (latent membrane protein) is seen in Sternberg-Reed (SR) cells and immunoblasts of AIDS-related lymphoma and infectious mononucleosis (IM). In HD, the region of the BNLF1 oncogene coding for the amino terminal and transmembrane domains (associated with oncogenic function) of LMP appears to be homogeneous whereas the region coding for the intracytoplasmic (carboxy terminal) domain of LMP is heterogeneous. Cytological similarities between SR cells and immunoblasts of IM and AIDS-related lymphomas are consistent with the hypothesis that the BNLF1 oncogene is one possible inducer of morphological features of SR cells. Whether chromosomal integration of EBV DNA is an important factor in activation of such a transforming activity remains to be elucidated. EBV DNA positive and negative HD cases with numerous SR cells lack significant mRNA expression of the two recombinase activating genes (RAG-1 and RAG-2). Therefore the SR cells appear to be derived from lymphocytes beyond the pre-B-cell or common thymocyte stage which may or may not subsequently become infected by EBV.
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PMID:Significance of the detection of Epstein-Barr virus DNA in lymph nodes in patients with Hodgkin's disease. 133 49


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