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. 2021 Apr 1;13(5):e13314. doi: 10.15252/emmm.202013314

Figure 4. Vs subverts HIV reactivation in U1 cells.

Figure 4

  1. Vs‐treated U1 cells were challenged with 5 ng/ml PMA or 1.25 μM prostratin (Pros) for 24 h, and HIV‐1 induction was monitored by gag RT–PCR. 10 mM NAC, an antioxidant known to subvert PMA mediated viral reactivation, was used as a positive control.
  2. Vs‐treated U1 cells were exposed to PMA, and viral activation was measured as a function of time, by gag RT–PCR. U1 cells were also treated with Vs or PMA alone.
  3. Untreated or Vs‐treated U1‐Orp1‐roGFP2 cells were exposed to PMA and the biosensor response was measured at the indicated time points. The biosensor response was also measured for untreated or PMA‐treated cells.
  4. J1.1 cells were treated twice with Vs for 15 min at 0 and 24 h time point. HIV‐1 induction was measured by gag RT–PCR at 24 h and 48 h post‐treatment. An untreated control was used for normalization.
  5. U1‐Grx1‐roGFP2 cells were serum starved for 30 min in the presence or absence of Vs and sodium selenite (0.5 nM), and the biosensor response was measured. Data were compared to serum‐starved control cells (C).
  6. U1 cells were either serum‐starved or supplemented with Se (0.5 nM) or Vs (0.62 ng/μl), and HIV reactivation was measured at 6 h post‐starvation by gag RT–PCR.

Data information: **P < 0.01, $/#/*P < 0.05, by Mann–Whitney test. Data are representative of results from three independent experiments performed in triplicate (mean ± SD).