Abstract
Studies presented here show that some functions of the human herpesvirus, EBV, may be transcriptionally differentially expressed in two cell types which carry the same (C15) isolate of this virus. Of the 'latent' viral functions investigated, only one (TP2) of the episomally-specific genes that encode terminal proteins (TP1 and TP2) is found to be expressed in the C15 epithelial cell tumour environment, whereas both are transcribed--as different, but related, messengers--in a B-cell line generated with virus from the C15 tumour. The other gene investigated is that for latent membrane protein (LMP), which is found in the same region of the EBV genome but on the opposite strand. This gene, apparently transcriptionally silent in B-cell (Burkitt's) lymphomas, is expressed in the C15 epithelial tumour, as well as in other nasopharyngeal carcinomas investigated. Promoter usage in the carcinomas and B-cells appears, in some cases at least, to be cell-type specific. Expression may also be governed by methylation since a chromosomally silent region in the carcinoma (that encompassing TP1) is highly methylated on CpG residues, whereas the active region (encoding TP2 and LMP) is virtually free of such methylation. Our data suggest that there may be selective transcriptional regulation of EBV genes in the two types of cells investigated. Thus, it may be unnecessary to invoke different virus genotypes to account for the two distinct malignancies--Burkitt's lymphoma and nasopharyngeal carcinoma--associated with EBV.
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