Extended Data Fig. 3: HIV infection results in the downregulation of proliferative pathways.
From: HIV infection reprogrammes CD4+ T cells for quiescence and entry into proviral latency
a., b. Pathway analysis (a) and transcription factor activity analysis (b) in +HIV αTCR 24 h cells indicate that many of the pathways upregulated during reactivation from quiescence correspond to those downregulated in +HIV 72 hpi cells. Numbers between parentheses indicate the number of genes in each gene list that drive the enrichment phenotype (see Methods). c. Most cyclin genes show a weak downregulation in +HIV 72 hpi cells and a much stronger one upon entry into full quiescence ( + HIV quiescent cells). Proliferation markers Ki67, CD71 and CD25 are included to indicate the extent of inhibition of proliferation. d. Relative to uninfected cells, unpurified HIV infected cells show decreased expression of cyclin D3 and Ki67, indicated by flow cytometry analysis performed at 2, 4 and 6 days post-infection. e. Mean fluorescence intensity of AF647 anti-Ki67 and PE anti-cyclin D3 signals detectable in uninfected and HIV infected cells over the course of 6 days. f. Following exposure of primary CD4 + T cells to HIV reporter virus, over half of the population becomes productively infected based on flow cytometry measurement of the level of expression of the GFP reporter gene. The values shown correspond to 2 days post infection. g. Viability of unpurified HIV infected cells relative to uninfected cells at 2, 4 and 6 days post-infection assessed using flow cytometry and Fixable Viability Dye eFluor™ 450.
