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. Author manuscript; available in PMC: 2011 May 1.
Published in final edited form as: Nat Immunol. 2010 Sep 26;11(11):1005–1013. doi: 10.1038/ni.1941

Fig. 2. HIV-stimulated IFN expression is IRF3-dependent.

Fig. 2

Wild type (WT), Trex1−/− (KO) or Trex1−/−Irf3−/− (DKO) primary MEFs were infected as in Fig. 1. (a) HIV-stimulated IFN-β induction, assessed by qRT-PCR 22 hpi, is eliminated in the absence of IRF3. (b) Irf3-deficiency partially rescues HIV infection in Trex1-deficient cells. HIV infection was measured by Luc activity 48 hpi. (c) Increased HIV autointegration in Trex1-deficient cells is not affected by Irf3-deficiency. Error bars indicate S.D. of at least three independent experiments. (d) IRF3 translocates to the nucleus in HIV-infected Trex1−/− cells. WT and Trex1−/− MEFs that were either uninfected or infected with HIV were stained 22 hpi for IRF3 (red) and DAPI (blue). (e) Expression of GFP from an HIV reporter virus (HIV-GFP) is reduced in Trex1−/− MEF compared to WT MEF. Flow cytometry analysis of GFP expression was measured 24 hpi. A representative plot from 3 independent experiments is shown.