       Document 0361
 DOCN  M9460361
 TI    Epstein-Barr virus latent and replicative gene expression in
       post-transplant lymphoproliferative disorders and AIDS-related
       non-Hodgkin's lymphomas.French Study Group of Pathology for
       HIV-associated Tumors.
 DT    9408
 AU    Rea D; Delecluse HJ; Hamilton-Dutoit SJ; Marelle L; Joab I; Edelman L;
       Finet JF; Raphael M; Departement d'Hematologie, Hopital
       Pitie-Salpetriere, Paris,; France.
 SO    Ann Oncol. 1994;5 Suppl 1:S113-6. Unique Identifier : AIDSLINE
       MED/94226932
 AB    In acquired immunodeficiency, B-cell proliferation is usually associated
       with Epstein-Barr virus (EBV), implying the impairment of the normal
       control of EBV and EBV-infected cells. It has been assumed that EBV
       infection is latent in lymphoproliferative disorders. In order to
       determine the type of latency and to investigate whether any
       lymphoproliferative disorders enter into the lytic cycle, we analyzed
       the expression of latent and replicative EBV genes in 9 post-transplant
       lymphoproliferative disorders (PTLD) and in 23 EBV-positive AIDS-related
       non-Hodgkin's lymphomas (AR-NHL). The PTLD cases were categorized into
       polyclonal or monoclonal polymorphic tumors and monoclonal monomorphic
       tumors. The AR-NHL cases included large-cell/immunoblastic (LC/IB) and
       Burkitt's lymphoma (BL) groups. We demonstrated that varying patterns of
       latent-viral-gene expression are exhibited showing the 3 forms of
       latency. Polymorphic PTLD and LC/IB AR-NHL frequently expressed type II
       or III latency, whereas monomorphic tumors and BL AR-NHL showed type I
       latency. It is noteworthy that 3 cases of BL AR-NHL expressed latency II
       form. Induction of lytic cycle highlighted by the expression of BZLF1
       occurred in 55.5% of PTLD, 36% of LC/IB and 22% of BL AR-NHL. In
       contrast, late viral proteins indicating productive cycle were present
       in 22% of PTLD, 14% of LC/IB, and were absent in BL cases. These data
       suggest that the impairment of EBV control permits disruption of
       latency, but the initiation of the lytic cycle may not always lead to
       viral production.
 DE    Gene Expression  Herpesvirus 4, Human/*GENETICS/PHYSIOLOGY  Human
       Lymphoma, AIDS-Related/*GENETICS  Lymphoproliferative
       Disorders/*GENETICS  Organ Transplantation/*ADVERSE EFFECTS  Support,
       Non-U.S. Gov't  Virus Latency/*GENETICS  Virus Replication/*GENETICS
       JOURNAL ARTICLE

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

