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
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
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
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
Stream transcription could be detected independently of the viral integration site. HIV-infected primary CD4+ T cells contain significant levels of transcription upstream of the 5'LTR To identify transcription upstream of the 5'LTR in HIV-infected peripheral blood lymphocytes (PBLs), we used the above method. After activation of HIV-infected PBLs with IL-2 and PHA, we rested them and isolated CD4+
M the two homologous alleles is possible. Nevertheless, these results are in a good agreement with the findings obtained by Northern blotting (Figures 1B and 1D). Taken together, the *mRNAs represent the host-viral chimeric transcripts, which contain sequences of the 5'LTR and terminate at its pA signals. In addition, RT-DqPCR revealed that levels of *mRNA exceed those of viral mRNA in unstimulate
One (Figure 7D, bars 2 and 6) and in combination with HMBA (Figure 7D, bars 3 and 7) or Tat (Figure 7D, bars 4 and 8) to levels in untreated cells (Figure 7D, bars 1 and 5). Interestingly, *mRNA levels decreased concomitantly with the increased activation of transcription from the 5'LTR in both cell lines. Probably, the formation of the PIC at the 5'LTR prevents elongating complex from the upstrea