Browsing by Subject "Epstein-Barr virus"

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    Analysis of Epstein-Barr virus strains and variants in classical Hodgkin s lymphoma by laser microdissection
    (Murcia : F. Hernández, 2008) García-Cosío, Mónica; Santón, Almudena; Martín, Paloma; Reguero, María Eugenia; Cristóbal, Eva; Bellas, Carmen
    Epstein-Barr virus (EBV) seems to have an etiological role in the pathogenesis of classical Hodgkin’s lymphoma (cHL). Studies of whole tissue DNA by polymerase-chain reaction (PCR) have shown a considerable number of cHL cases with co-infections by different EBV strains and variants, which apparently contradict the clonality of EBV in cHL previously demonstrated by Southern blot analysis. Due to the paucity of HRS cells in HL tissues, studies on single cell DNA are necessary to identify the specific cellular location (HRS cells and/or bystander B lymphocytes) of the EBV strains and variants present in tissue specimens. In the current study, the presence of EBV was determined by PCR of the 3’ end of the LMP-1 gene and EBNA-3C gene in whole tissue and, consecutively, in isolated cells from 26 cases of cHL: 10 HIV-positive and 16 sporadic cHL cases. EBV EBERs were present in all but 2 sporadic cHL cases, which were used as negative controls. At isolated cell level, EBNA-3C gene PCR was more sensitive. Indeed, from the cHL cases in which dual-infection was present, it was observed that, in most of them, HRS cells were infected by type 1 virus, and B lymphocytes were co-infected by both types, which points towards EBV infection occurring early in cHL development. Moreover, the finding of 2 cases with dual-infection in HRS may suggest that, in a small percentage of cHL cases, HRS cells derive from different neoplastic clones, or that HRS cells are superinfected by other viral types after the establishment of the neoplastic clone.
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    Down regulation of gastric and intestinal phenotypic expression in Epstein-Barr virus-associated stomach cancers
    (Murcia : F. Hernández, 2007) Hirano, N.; Tsukamoto, T.; Mizoshita, T.; Koriyama, C.; Akiba, S.; Campos, F.; Carrasquilla, G.; Carrascal Marino, E.; Cao, X.; Toyoda, T.; Ban, H.; Miki, K.; Tatematsu, M.
    importance of gastric and intestinal phenotypic expression for stomach carcinogenesis. In this study, we focused on Epstein-Barr virus (EBV)-associated stomach cancers, with special attention to Cdx2. Methods and Results: We evaluated the expression of gastric and intestinal phenotypic markers by immunohistochemistry in 35 EBV-positive [EBV (+)] and 75 EBV-negative [EBV (-)] stomach cancers in Colombia. The lesions were divided phenotypically into gastric (G), gastric-and-intestinal mixed (GI), intestinal (I), and null (N) phenotypes. In the EBV (+) cases, the lesions were divided phenotypically into 9 G (25.7%), 1 GI (2.9%), 3 I (8.6%), and 22 N (62.9%) types. Similarly, the EBV (-) lesions were also classified phenotypically as 15 G (20.0%), 19 GI (25.3%), 24 I (32.0%), and 17 N (22.7%) types. The proportion of N type EBV (+) lesions was higher than for their EBV (-) counterparts (P<0.0001). The expression of Cdx2 and MUC2 was also found to be significantly lower in EBV (+) than in EBV (-) stomach cancers (P=0.0001; P<0.0001). Cdx2 expression in the intestinal metaplastic glands present in non-neoplastic mucosa surrounding EBV (+) lesions was also significantly lower than in EBV (-) tumors (P=0.016) despite no evidence of EBV infection by low expression of intestinal phenotype markers, including Cdx2, and only occasional gastric phenotypic expression.
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    hu-PBL-SCID mice: an in vivo model of Epstein-Barr virus-dependent lymphoproliferative disease
    (Murcia : F. Hernández, 1998) Fuzzati-Armentero, M.T.; Duchosal, M.A.
    The Epstein-Barr virus (EBV) exists in most huni:tns as a lifelong latent infection established in host B cells after a primary viral encounter. In immunosuppressed intlivitluals, such as post-transpl~rnt patients, the presence of EBV-infected B cells may lcad to Iq'niplloproliferative disease. Injection of human peripheral blood lymphocytes from EBV-positive clonors into mice wit h severe combined immunodeficiency induces human lymphoproliferative disease i n the recipient closely resembling that of human posttransplant patients. This xenochimeric human-mouse model is increasingly being used to elucidwrc the mcchnnisms of EBV-specific lymphomagenesis and to assess novel therapeutic approaches.