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. 2019 Jun 11;16:15. doi: 10.1186/s12977-019-0477-y

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© The Author(s) 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 2 — LentiCRISPR/SaCas9 mediated cleavage of CCR5 in TZM-bl cells against HIV-1 infection. a LentiCRISPR/SaCas9 editing of the CCR5 gene in TZM-bl cells. sgRNA-#6, #8 or control were transfected into TZM-bl cells delivered by lentiviral vector. Three days post transduction, genomic DNA was extracted and T7E1 assay was conducted. b Detection of CCR5 expression in TZM-bl cells by flow cytometry. c Sanger sequencing of CCR5 target loci in the TZM-bl cells modified by LentiCRISPR-SaCas9/sgRNA. d Disruption of CCR5 in TZM-bl cells could render cell resistance to HIV-1 infection. The cells were transduced with LentiCRISPR-SaCas9/sgRNA-#6, #8 or control. Then the modified cells were infected with HIV-1_YU2 (MOI = 0.5). Luciferase reporter assay was performed to analyze infection efficiency. Data were analyzed by unpaired t-test and error bars showed the mean ± SEM of three independent experiments (*p < 0.05; **p < 0.01; ***p < 0.001)