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. 2020 Jun 29;17:16. doi: 10.1186/s12977-020-00524-2

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.

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Fig. 4 — CPSF6 is essential for MxB to inhibit HIV-1 nuclear import in target cells. Primary MDMs (a) and CD4⁺ T cells (b) isolated from three independent donors were transduced with concentrated lentivirus overexpressing MxB or a control lentivirus (Ctrl) for 72 h, then cells were transfected with CPSF6 siRNA (siCPSF6) either negative control (siNC). 24 h after siRNA transfection, cells were challenged with HIV-1_Bal or HIV-1_NL4-3. The level of of MxB, CPSF6, Gag and HIV-1 DNA was determined 48 h post infection. The mean ± SD of three technical replicates were shown for each donor