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. 2015 Jun 18;12:51. doi: 10.1186/s12977-015-0178-0

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© Savarino and Shytaj 2015

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/http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Mechanistic model of HIV-induced persistent immune-activation. a HIV enters CD4-expressing plasmacytoid dendritic cells (pDCs); b the virus is endocytosed, decapsided and its RNA is recognized by toll-like receptor 7 (TLR-7); c stimulation of TLR-7 prompts a signaling cascade inducing IFN-α transcription in the nucleus; d production of IFN-α favors activation of several cell subsets such as T, B and natural killer (NK) lymphocytes. Chloroquine (CQ) is postulated to reduce the efficiency of this mechanism by accumulating in endosomes and decreasing HIV-mediated TLR-7 signaling [44].