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Figure 2 | Virology Journal

Figure 2

From: Evidence that the Nijmegen breakage syndrome protein, an early sensor of double-strand DNA breaks (DSB), is involved in HIV-1 post-integration repair by recruiting the ataxia telangiectasia-mutated kinase in a process similar to, but distinct from, cellular DSB repair

Figure 2

NBS1 is required for efficient HIV-1 transduction of primary cells. (A) NBS1-deficient fibroblasts (GM07166) and matched controls (GM04506) were infected with HIV-1-based vector carrying the lac Z reporter at an m.o.i. of 0.25. Five and seven days post infection (dpi) cells were stained using a β-galactosidase assay (Stratagene protocol) and transduced (blue) cells were counted under a light microscope the following day. Light grey – NBS1-deficient cells; dark grey – normal cells. The error bars represent standard deviation, p = 0.029 for 5 dpi and 0.021 for 7 dpi. (B) Light microscopic images from the same experiment as in A. (C) The effect of the NBS1 deficiency on expression of the lac Z marker. The NBS1-deficient and control cells were transfected with the lac Z plasmid and lac Z-expressing cells were counted three days post transfection. Six randomly selected fields were counted per each point. The error bars represent standard deviation. The differences were not statistically significant (p > 0.2) (D) Transduction with the HIV-1-based vector carrying the EGFP marker. NBS1-deficient and control fibroblasts were infected with the vector and transduced cells were counted by flow cytometry at multiple time points (2–7 dpi). Results from 7 dpi are shown. Histograms of mock infected cells (top) and cells infected at an m.o.i. of 0.1 (bottom) are shown. As seen in the gated regions, 13.45% of control fibroblasts were stably transduced, whereas transduction of NBS fibroblasts was only 4.79%.

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Virology Journal

ISSN: 1743-422X