Lation than the 5'LTR, suggesting that the latter LTR is much stronger subjected to TI. Even if there is transcription from host gene `reading through' both LTRs in some latent cells, this does not diminish the impact of TI on the 5'LTR.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptCell Host Microbe. Author manuscript; available in PMC 2014 November 03.Lenasi et al.Page
Lation than the 5'LTR, suggesting that the latter LTR is much stronger subjected to TI. Even if there is transcription from host gene `reading through' both LTRs in some latent cells, this does not diminish the impact of TI on the 5'LTR.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptCell Host Microbe. Author manuscript; available in PMC 2014 November 03.Lenasi et al.Page
Lation than the 5'LTR, suggesting that the latter LTR is much stronger subjected to TI. Even if there is transcription from host gene `reading through' both LTRs in some latent cells, this does not diminish the impact of TI on the 5'LTR.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptCell Host Microbe. Author manuscript; available in PMC 2014 November 03.Lenasi et al.Page
Me transcription through the provirus, since slight enrichment of elongating RNAPII in the HIV coding region of transcriptionally silent J-Lat 9.2 cells was observed using ChIPqPCR assay. However, transcription originating from the host promoter, ignoring pA sites in both LTRs and consequently splicing out the provirus together with the host intron (Han et al., 2004) is most likely less frequent t
K of the latent provirus in J-Lat 9.2 cells is TI of the 5'LTR caused by the transcription of the host PP5* gene. This interfering transcription results in the lack of Sp1 and the presence of the elongating RNAPII at the 5'LTR. Moreover, TI can be partially rescued by TNF- stimulation, as documented by the appearance of Sp1 and initiating RNAPII at the 5'LTR. The slight enrichment of the RNAPII in
K of the latent provirus in J-Lat 9.2 cells is TI of the 5'LTR caused by the transcription of the host PP5* gene. This interfering transcription results in the lack of Sp1 and the presence of the elongating RNAPII at the 5'LTR. Moreover, TI can be partially rescued by TNF- stimulation, as documented by the appearance of Sp1 and initiating RNAPII at the 5'LTR. The slight enrichment of the RNAPII in
Nce it has been demonstrated that transcription from the PP5 promoter could be reduced through inhibiting estrogen receptor (ER) (Urban et al., 2001). Therefore, we established J-Lat 9.2 and control J-Lat 8.4 cell lines that stably express miRNA-adapted shRNA (shRNAmir) against the ER mRNA (J-Lat 9.2 shER and J-Lat 8.4 shER, respectively). In both J-Lat shER cell lines, the ER levels were decrease
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