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
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