FIG. 6.

The BaLCV and RhLCV Qp promoters are functional within latently infected B lymphocytes. RT-PCR analysis was employed to detect, and distinguish between, Qp- and Fp-specific EBNA-1 gene transcription in S594 (BaLCV-infected) and Mm278LCL (RhLCV-infected) cells. The exon structure of an EBNA-1 mRNA (not to scale) derived from either Fp (active during lytic infection) or Qp is illustrated at the bottom; Fp and Qp transcription start sites (bent arrows) and the relative annealing sites of the oligonucleotide primers used for RT and subsequent amplification of cDNAs by PCR are depicted with respect to the mRNA structure. The upper two panels demonstrate detection of Qp-specific EBNA-1 transcription in latently infected BL cells (Akata), in which Fp is silent, and detection of Fp activity in lytically infected BL cells (P3HR-1 BL cells treated with 12-O-tetradecanoylphorbol-13-acetate and sodium butyrate), respectively. By comparison, the predominate origin of EBNA-1 transcription detected in the BaLCV- and RhLCV-infected cells was attributable to Qp. PCR products were detected by Southern blot hybridization with an EBV, BaLCV, or RhLCV cDNA probe that had been generated by the respective SP3-E1 primer pair and sequenced to confirm that they were EBNA-1 cDNAs. +/−, presence and absence, respectively, of reverse transcriptase in the cDNA synthesis reaction.