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
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
Es obtained with the LTR-specific primers represent a sum of transcripts originating from the host promoter and of viral transcripts, which also contain LTR sequence at their 3' ends. Therefore, the measured ratio corresponds to the equation a+b/b, where `a' is the number of host-viral chimeric transcripts and `b' the number of viral transcripts (see Supplemental text 2). First, we determined this
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
Es 3B and S3). We decided to use this cell line because of a smaller ratio between HIV transcripts and *mRNA in these cells compared to those in J-Lat 9.2 cells (Figure 2D, bars 3 and 4). The ratio between LTRand Rev-containing transcripts increased with the decreased levels of viral expression consistent with the rational equation (see Supplemental text 2), and revealed that the upstream transcri
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
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
Es obtained with the LTR-specific primers represent a sum of transcripts originating from the host promoter and of viral transcripts, which also contain LTR sequence at their 3' ends. Therefore, the measured ratio corresponds to the equation a+b/b, where `a' is the number of host-viral chimeric transcripts and `b' the number of viral transcripts (see Supplemental text 2). First, we determined this