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Immunohistology of Epstein-Barr virus-associated antigens in B cell disorders from immunocompromised individuals.
Thomas, J A; Hotchin, N A; Allday, M J; Amlot, P; Rose, M; Yacoub, M; Crawford, D H.
Afiliação
  • Thomas JA; Histopathology Unit, Imperial Cancer Research Fund, London, United Kingdom.
Transplantation ; 49(5): 944-53, 1990 May.
Article em En | MEDLINE | ID: mdl-2159663
ABSTRACT
Proliferating B cell lesions developing in a series of immunosuppressed organ transplant recipients and patients with X-linked lymphoproliferative syndrome were examined for Epstein-Barr virus and cellular gene expression using immunocytochemistry and immunoblotting techniques. Results indicate that all the lesions examined from the patients in this series expressed Epstein-Barr virus gene products that were consistent with a latent, nonproductive type of infection. No lytic cycle antigens associated with productive viral infection were detected. This pattern is similar to the viral gene expression in normal B cells immortalized by Epstein-Barr virus in vitro. The demonstration in this study of Epstein-Barr virus viral gene expression in posttransplant and X-linked proliferative syndrome B cell disorders provides important new evidence for the primary role of Epstein-Barr virus in the development of these lesions. This is in contrast to the subsidiary role that the Epstein-Barr virus has in the etiology of Burkitt's lymphoma.
Assuntos
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Linfócitos B / Herpesvirus Humano 4 / Transtornos Linfoproliferativos / Antígenos Virais Tipo de estudo: Risk_factors_studies Limite: Humans Idioma: En Revista: Transplantation Ano de publicação: 1990 Tipo de documento: Article País de afiliação: Reino Unido
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Linfócitos B / Herpesvirus Humano 4 / Transtornos Linfoproliferativos / Antígenos Virais Tipo de estudo: Risk_factors_studies Limite: Humans Idioma: En Revista: Transplantation Ano de publicação: 1990 Tipo de documento: Article País de afiliação: Reino Unido