       Document 0723
 DOCN  M9620723
 TI    Production of inflammatory cytokines by Epstein-Barr virus
       (EBV)-infected lymphoblastoid cell lines spontaneously originated from
       the peripheral blood of patients with human immunodeficiency virus (HIV)
       infection.
 DT    9602
 AU    Roncella S; Baldi L; Cutrona G; Viale M; Rizzo F; Gasco M; Ferrarini M;
       Pistoia V; Services of Clinical Immunology, National Institute for
       Cancer; Research, Genoa, Italy.
 SO    Clin Immunol Immunopathol. 1995 Nov;77(2):162-71. Unique Identifier :
       AIDSLINE MED/96036726
 AB    In this study we have raised spontaneous Epstein-Barr virus
       (EBV)-positive lymphoblastoid cell lines (LCL) from the peripheral blood
       of human immunodeficiency virus (HIV)-infected individuals and of
       control patients with primary EBV infections. These LCLs were also
       raised in the presence of the viral inhibitor phosphonoformate (PFA);
       under these conditions, the in vitro infection of bystander B
       lymphocytes with EBV released in culture by in vivo infected B cells is
       inhibited. Thus, the latter LCLs are likely to represent the progeny of
       B cells latently infected by EBV in vivo. The LCLs raised in the
       presence or absence of PFA had the same phenotypic features, type of EBV
       latency, and growth pattern irrespective of whether they had been raised
       from HIV-seropositive individuals or patients with primary EBV
       infections or had been generated by infecting normal B cells in vitro.
       Studies on the production of inflammatory cytokines were conducted by
       Northern blotting or by determining the cytokine concentrations in the
       cell supernatants by immunoassays or bioassays. Three of eight LCLs from
       HIV-seropositive patients released TNF alpha and 5/5 released TNF beta,
       IL6 was present in the supernatants of 1/8 LCLs, and IL1 alpha and IL1
       beta were not detected in any culture supernatant. No differences were
       noticed in the patterns of cytokine secretion among the LCLs from
       HIV-seropositive patients and in those raised from patients with primary
       EBV infections or obtained by infecting normal B cells in vitro with
       EBV. It is tempting to speculate that abnormally expanded EBV-harboring
       B cells in HIV-seropositive patients may participate in the pathogenesis
       of certain clinical manifestations by releasing inflammatory cytokines;
       some of these cytokines might also contribute to the in vivo spreading
       of HIV infection. However, the spontaneous LCLs from HIV-seropositive
       individuals do not display abnormal features compared to latently
       EBV-infected LCLs from other sources despite the high frequency of
       EBV-driven lymphoproliferative disorders observed in AIDS patients.
 DE    Adult  Cell Line  Cytokines/*BIOSYNTHESIS/IMMUNOLOGY  Female  Flow
       Cytometry  Herpesvirus 4, Human/*ISOLATION & PURIF  Human  HIV
       Infections/*BLOOD/IMMUNOLOGY  Immunophenotyping
       Lymphocytes/*IMMUNOLOGY/PATHOLOGY/*VIROLOGY  Male  RNA,
       Messenger/BIOSYNTHESIS  Support, Non-U.S. Gov't  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

