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
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
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
T the level of gene expression act cooperatively to establish and maintain HIV latency. In conclusion, our study reveals that TI represents a key mechanism that antagonizes proviral gene expression to promote the latency of HIV. Furthermore, it demonstrates several means that could be used to counteract TI for reactivating latent HIV. Future mechanistic studies linking TI and other transcriptional
Mpared GFP expression of parental and J-Lat shER cells using fluorescence activated cell sorting (FACS). As expected, no GFP-expressing cells could be detected in untreated cells (Figures 6C-6F, mock). About 20 of cells turned GFP-positive in TNF--treated J-Lat 9.2 cells (Figure 6C, TNF-). Importantly, the inhibition of PP5 transcription synergized with TNF- to increase further the number of GFP-
Ated for animals receiving no antibodies. The plasma neutralization titer was also determined for each of the MAb recipients at multiple times post infusion (Figure 4a). The median plasma neutralizing titers for the four groups of macaques at the time of SHIVAD8-EO acquisition were low: