Nasal NK- and T-cell lymphomas share the same type of Epstein-Barr virus latency as nasopharyngeal carcinoma and Hodgkin's disease

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Abstract
Nasal T/NK‐cell lymphomas can be further separated into those of natural killer (NK) cell lineage or of T‐cell lineage, with differences in cellular phenotype, T‐cell receptor (TcR) gene rearrangement and TcR transcript expression. Both NK‐ and T‐cell subtypes are closely associated with Epstein‐Barr virus (EBV). In this study, EBV gene expression was determined in 23 cases of nasal lymphoma (NL) by in situ hybridisation (ISH), reverse transcriptase‐polymerase chain reaction (RT‐PCR) and immunohistochemistry (IH). Of the 23 cases, 19 were classified as NK‐cell and 4 as T‐cell tumours. ISH for EBV‐encoded small non‐polyadenylated RNAs showed that all cases, whether NK or T, harboured EBV in virtually all tumour cells. RT‐PCR demonstrated that NL of both subtypes expressed EBNAI of the QUK splice pattern, the latent membrane proteins, LMPI and 2 and the BamHI A rightward transcripts in the absence of EBNA2 mRNAs, compatible with the latency type II pattern. In addition, analysis of EBV protein expression by IH revealed a heterogeneous pattern of EBV gene expression at the single‐cell level consisting of both LMPI+ and LMPI‐ tumour cells, suggesting a mixture of latency I and II. Although 2 early lytic transcripts, BZLFI and BHRFI, were also detected in 13 and 10 cases, respectively, the lack of ZEBRA staining in any case indicates that these lytic transcripts are most likely expressed by rare cells in the biopsies entering lytic cycle. The viral transcriptional pattern similar to that of nasopharyngeal carcinoma and Hodgkin's disease suggests that EBV can exploit common regulatory mechanisms for gene transcription in diverse host cell types. Down‐regulation of immunogenic proteins (EBNA2‐EBNA6) in nasal lymphoma may enable tumour cells to evade host cytotoxic T‐cell surveillance. © 1996 Wiley‐Liss, Inc.

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