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
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
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
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
Tion at the time of each challenge using a probit regression model. The fitted probabilities from the models are plotted separately for each MAb group, with the estimated probability of infection for the control animals (0.27) indicated by the open circle adjacent to each ordinate. The VRC01 and VRC01-LS curves are superimposed. The points on each curve represent the median concentration at the ti
D DataExtended Data Figure 1. Neutralization sensitivity of SHIVAD8-EO to four broadly acting neutralizing anti-HIV-1 MAbsa, Neutralizing activity of the indicated bNAbs was determined against SHIVAD8-EO pseudovirions using TZM-bl target cells. The calculated IC50 and IC80 values are shown atNature. Author manuscript; available in PMC 2016 November 29.Gautam et al.Pagethe bottom. b, Neutralizing a
D DataExtended Data Figure 1. Neutralization sensitivity of SHIVAD8-EO to four broadly acting neutralizing anti-HIV-1 MAbsa, Neutralizing activity of the indicated bNAbs was determined against SHIVAD8-EO pseudovirions using TZM-bl target cells. The calculated IC50 and IC80 values are shown atNature. Author manuscript; available in PMC 2016 November 29.Gautam et al.Pagethe bottom. b, Neutralizing a
Ly on clinical criteria, there was a selection bias towards more advanced immunodeficiency at baseline, which increases the risk of drug resistance. However, these biases reflect the realities in many African ART programmes.2 ?4,10,11 Finally, this was a cross-sectional survey of patients alive and in care, leaving out a high number of patients who died, were lost to follow-up or transferred out;