Epstein-Barr virus (EBV) latent and replicative gene expression in AIDS-related non-Hodgkin's lymphoma (NHL) and post-transplant lymphoproliferative disorders (PTLD) (Meeting abstract).

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Epstein-Barr virus (EBV) latent and replicative gene expression in AIDS-related non-Hodgkin's lymphoma (NHL) and post-transplant lymphoproliferative disorders (PTLD) (Meeting abstract).

Fifth International Conference on Malignant Lymphoma, June 9-12, 1993, Lugano, Switzerland, p. 22, 1993.. Unique Identifier : AIDSLINE ICDB/95606900
Rea D; Delecluse HJ; Hamilton Dutoit SJ; Joab I; Young L; Raphael M; Centre d'Ecologie Cellulaire, Dept. of Hematology, Pitie; Salpetriere, Paris, France

Abstract: NHL and PTLD arising in the setting of immunodeficiency states such as HIV infection and organ transplantation are frequently associated with EBV. Three forms of latent infection have been described in vitro. In type I latency (LMP-, EBNA2-) only EBNA1 is expressed. In type II latency (LMP+, EBNA2-), EBNA1 and LMP are detected. In type III latency (LMP+, EBNA2+) the 6 EBNAs (1, 2, 3A, 3B, LP, 3C) and the 3 LMPs (1, 2A/2B) are expressed. Furthermore, EBV replicative cycle can be activated from latent-infected cells. In order to investigate EBV cycle in vivo, the pattern of EBV latent and replicative gene expression was analyzed in, respectively, 18 and 9 EBV positive AIDS-related NHL and PTLD. EBV status was determined either by Southern blot with the BamHI W probe or with the EBER1 riboprobe. EBV latent and replicative proteins were detected by the immunoperoxidase and the alkaline phosphatase anti-alkaline phosphatase techniques. The following monoclonal antibodies were used: Cs1-4 and PE2 directed against the latent proteins LMP1 and EBNA2, BZ1 directed against the immediate early replicative protein BZLF1, F3.23, H667 and 65 directed against the late proteins VCA, MA and BCRF1. Histologic subtypes of AIDS-related NHL included 10 large cell NHL (LCL) and 8 BL. PTLD consisted of 4 polymorphic polyclonal cases (PP), 3 polymorphic monoclonal cases (PM) and 2 monomorphic monoclonal cases (MM). In AIDS-related NHL, the 3 forms of latent infection were detected in LCL, whereas BL more often expressed type I latency. A few proportion of BL showed type II latency but failed to express type III latency. In PTLD, polymorphic proliferations expressed the 3 types of latency, whereas MM only showed type I latency. Replicative proteins were present in 5 LCL and 1 BL which all expressed the BZLF1 protein, indicating a switch from latency to replication. However, late viral proteins were not detected in BL and VCA was detected in 2 LCL without expression of other late viral proteins. In PTLD, BZLF1 was detected in 5 polymorphic cases but only 2 cases expressed late viral proteins. MM failed to express EBV replicative proteins. Our results indicate that the 3 forms of latent infection are represented in vivo in AIDS-related NHL and PTLD. LCL and polymorphic PTLD frequently express type II or type III latency, whereas BL and MM show more often type I latency. Noteworthy, latency II is observed in a few proportion of BL. EBV replicative cycle occur in a great proportion of cases. However, the initiation of EBV replicative cycle may not always lead to viral production. Further studies should be undertaken to better understand the role of EBV replication in malignant cells in AIDS-related NHL and PTLD.

Keywords: Antigens, Viral/GENETICS/METABOLISM DNA-Binding Proteins/GENETICS/METABOLISM Gene Expression Herpesvirus 4, Human/PHYSIOLOGY Human Lymphoma, AIDS-Related/*GENETICS/METABOLISM Lymphoproliferative Disorders/ETIOLOGY/*GENETICS/METABOLISM RNA-Binding Proteins/GENETICS/METABOLISM Trans-Activators/GENETICS/METABOLISM Viral Matrix Proteins/GENETICS/METABOLISM Viral Proteins/GENETICS/METABOLISM Virus Replication ABSTRACT
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