LACK OF THE EXPRESSION OF EBNA-2 AND LMP-1 IN T-CELL NEOPLASMS POSSESSING EPSTEIN-BARR-VIRUS

We investigated 34 cases of T-cell neoplasm [15 cases of T-cell granul ar lymphocytic leukemia (T-GLL), 10 cases of T-cell non-Hodgkin's lymp homa (T-NHL), six cases of T-cell chronic lymphocytic leukemia (T-CLL) , and three cases of cutaneous T-cell lymphoma] to study their associa tion with Epstein-Barr virus (EBV). In 4 (three T-NHL and one T-GLL) o f 34 cases, EBV genome was detected in a single episomal form, while p olyclonal EBV-DNA was detected in one (T-NHL) of the remaining cases. All three cases of T-NHL having monoclonal EBV episome showed histolog ically diffuse large-cell lymphoma and developed leukemic conversion. Phenotypic analysis showed that two of these four cases were CD4+, CD8 -, and the remaining two cases were CD4-, CD8+. The cells from all fou r cases were confirmed to be in T-cell lineage by detecting the rearra ngement of T-cell receptor (TCR) beta or gamma chain gene. By reverse transcription-polymerase chain reaction (RT-PCR), EBNA-1 was detected at low levels, and neither EBNA-2 nor LMP-1 were found in any of the t hree cases examined. Lack of the expression of EBNA-2 and LMP-1 was al so confirmed by immunocytochemical staining. The cells of these four c ases did not show rearrangement or overexpression of c-myc and bcl-2 g enes by Southern and Northern blots, and the mutation of p53 gene was detected in only one patient. These results suggest that other latent gene products of EBV or other cellular oncogenes are involved in the d evelopment of Japanese T-cell neoplasm after EBV infection. (C) 1995 b y The American Society of Hematology.