R (1.825 and 6.446 g/ml) and were also in the same range as the IC80 values determined in vitro. It is worth noting that three of the six recipients of the 10-1074 MAb experienced rapid decay of plasma antibody, which fell to background levels between weeks 4 to 6 following administration (Fig. 3c). A similar pattern occurred for three of the 3BNC117 MAb and VRC01-LS recipients, although the decli
R (1.825 and 6.446 g/ml) and were also in the same range as the IC80 values determined in vitro. It is worth noting that three of the six recipients of the 10-1074 MAb experienced rapid decay of plasma antibody, which fell to background levels between weeks 4 to 6 following administration (Fig. 3c). A similar pattern occurred for three of the 3BNC117 MAb and VRC01-LS recipients, although the decli
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
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