Fections in the recipients of the VRC01, 3BNC117, 10-1074 and VRC01-LS MAbs than in the control animals (P = 0.007, 0.002, 0.002 and 0.002, respectively), using the Wilcoxon Rank Sum test (Fig. 2b). A comparison of the individual pairs of Kaplan-Meier curves revealed that 10-1074, 3BNC117 and VRC01-LS were not significantly different from each other in blocking infection. Ultrasensitive nested qRT
For assistance with writing the manuscript, and members of Peterlin laboratory for helpful discussions and continuous support. This work was supported by grants from the National Institutes of Health to B.M.P. (AI49104 and AI058708). T.L. was supported in part by a grant from the National Institutes of Health, University of California San Francisco ladstone Institute of Virology Immunology Cente
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
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
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
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
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