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. 2016 Mar 29;13:22. doi: 10.1186/s12977-016-0255-z

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© Tsao et al. 2016

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. 4 — CCR5 agonist MIP-1β enhances R3A-5/6AA pathogenesis to promote bystander CD4 T cell depletion PBMCs were infected with R3A-5/6AA virus and treated with recombinant MIP-1 β (200 ng/mL) at 3 h post infection. At 6 days post infection, viabilities of p24(−) and p24(+) CD4 T cell were measured as described in Fig. 1c. a Representative FACS plots and b graphical summary are presented. c %CD4 T cells survival at 6 days post infection was measured by gating on live CD8(−) CD3(+) cells. *p < 0.05