Ly 20 activation of viral transcription (see Figure 7) already precludes detection of the upstream transcription. This finding is not surprising, as we demonstrated that there is 11-fold or 38-fold more viral mRNA than *mRNA in TNF- treated cells (Figure 2D, bars 3 and 4). Predictably, our control experiments demonstrate that the ratio between the Rev- and Env-containing transcripts was 1 in untr
Ly 20 activation of viral transcription (see Figure 7) already precludes detection of the upstream transcription. This finding is not surprising, as we demonstrated that there is 11-fold or 38-fold more viral mRNA than *mRNA in TNF- treated cells (Figure 2D, bars 3 and 4). Predictably, our control experiments demonstrate that the ratio between the Rev- and Env-containing transcripts was 1 in untr
Tream of the 5'LTR Existence of the host-viral chimeric transcripts that originate from a host promoter and include 5'LTR could be useful for identifying ongoing transcription upstream of the 5'LTR independently of the site of viral integration. Therefore, we next devised an assay, which determines the ratio between transcripts containing LTR sequences and those containing sequences present solely
Tream of the 5'LTR Existence of the host-viral chimeric transcripts that originate from a host promoter and include 5'LTR could be useful for identifying ongoing transcription upstream of the 5'LTR independently of the site of viral integration. Therefore, we next devised an assay, which determines the ratio between transcripts containing LTR sequences and those containing sequences present solely
Nificant levels of the host-viral chimeric transcripts. Because they indicate active transcription upstream of the 5'LTR, these findings suggest that viral transcription is subjected to TI in these cells. Transcriptional interference by the actively transcribed host gene reverses viral transcription from the 5' to the 3'LTR Next, we investigated in detail how active transcription of the upstream P
King place in latent J-Lat 9.2 and 15.4 cell lines, in which the ongoing transcription from the host gene would interfere with transcription from the 5'LTR. Consequently, due to the premature termination of *mRNA at the pA site in the 5'LTR, the 3'LTR would no longer be subjected to TI and could thus be activated. To test this hypothesis, we activated viral gene expression with Tat or TNF- and com
Ly 20 activation of viral transcription (see Figure 7) already precludes detection of the upstream transcription. This finding is not surprising, as we demonstrated that there is 11-fold or 38-fold more viral mRNA than *mRNA in TNF- treated cells (Figure 2D, bars 3 and 4). Predictably, our control experiments demonstrate that the ratio between the Rev- and Env-containing transcripts was 1 in untr
Vels of viral particles, we speculate that average levels of host-viral chimeric transcripts in these cells exceed those in the two J-Lat cell lines. These results thus suggest that TI plays a key role in primary CD4+ T cells. In J-Lat 9.2 and 15.4 cells, the host-viral chimeric transcripts terminated at the pA site in the 5'LTR, but transcripts initiating at the host promoter and terminating at t