The BamHI H fragment of Marek's disease virus (MDV), which has been hypothesized to contain a tumor-inducing gene, was partially sequenced and analyzed for transcriptional activity. Transcription of several RNAs was found to initiate within BamHI-H, with the major transcripts initiating on either side of a putative MDV origin of lytic replication. A 1.8-kilobase gene family found to be produced only by pathogenic MDV was detected, and its transcription map was produced. It is hypothesized that the 1.8-kilobase gene family is directly associated with the tumorigenic potential of MDV.

We used nuclease digestion to map RNA transcripts encoded in the BamHI M fragment of the Epstein-Barr virus (EBV) genome (strain B95-8). Of the five RNAs, three are rightwardly transcribed, have different cap sites but common 3' termini, and are unspliced. The two remaining RNAs are leftwardly transcribed and are 5' and 3' coterminal. One of these transcripts is spliced, resulting in the removal of a small intron from the 5' region of this RNA. We have previously published data which indicated that the BamHI M region is the first actively transcribed region of the viral genome during the replicative cycle, suggesting that one or more genes in this region is important in the initiation of EBV replication. We have now mapped two large EcoRI restriction fragments which span approximately 75% of the P3HR-1 defective genome and which contain DNA from the BamHI M region of the standard genome. The data indicate that only the coding and 5' flanking sequences for the leftwardly transcribed RNAs are intact within the defective genome. Fewer than 500 bases coding for the 3'-most regions of the rightwardly transcribed RNAs are intact, and it is unlikely that these encode functional native polypeptides. Therefore, it seems that transcriptional activation of the BamHI M-region genes is not mediated directly by the rearrangement of M genes in defective P3HR-1 EBV.

The attenuation of Marek's disease virus (MDV) is associated with loss of pathogenicity and tumorigenicity. Previous studies have demonstrated a strong correlation between attenuation and amplification of a specific sequence located within the MDV terminal and internal repeats. We recently reported that the regions containing the amplified sequences, the BamHI D and H fragments, were transcriptionally active. However, differential transcription activity was observed to exist between attenuated and pathogenic MDV strains. Specifically, a major transcript of 1.8 kilobases was found to be produced by pathogenic MDV and not by attenuated MDV. We now report that the disappearance of this transcript is concomitant with the production of a 0.4-kilobase RNA, an RNA resulting from the truncation of the tumorigenicity-related transcript.

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