Fig. 6: A loss-of-function mutation within the Rev gene does not abolish the quiescence-inducing capacity of HIV.
From: HIV infection reprogrammes CD4+ T cells for quiescence and entry into proviral latency
a, Ex vivo infection of Th17 polarized primary CD4+ T cells from 2 healthy donors with a Rev mutant HIV construct results in loss of cyclin D3 and Ki67 expression within 48 h. This indicates that Tat and/or Nef, which are the only genes still expressed by this construct, are critical for the induction of the HIV-induced quiescence programme. b, The Rev mutant HIV construct induces the same level of drop in Ki67 as the parental construct with a functional Rev in 48-hpi ex vivo-infected CD4+ T cell populations from 2 healthy donors. The ratio of cells with high versus low levels of Ki67 as shown by flow cytometry is plotted on the Y axis. In this panel and in c, the values shown are the mean ± s.d. of biological replicates. c, Mean fluorescence intensity of PE anti-cyclin D3 signal detectable in uninfected cells and cells infected with wild-type or mutant Rev HIV constructs at 48 hpi from 2 healthy donors indicates a similar level of loss of proliferative state. d, Flow cytometry results represented as a histogram show the bimodal pattern of expression of Ki67 at 48 hpi in ex vivo-infected cells from 2 healthy donors, consistent with the activation of the HIV-induced quiescence programme in the Rev mutant HIV construct.
