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. 2019 Aug 29;9:12552. doi: 10.1038/s41598-019-49056-6

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© The Author(s) 2019

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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TGF-β1 mediates HIV suppression via BLIMP-1 and histone deacetylases. NHBE ALI cultures were treated with TGF-β1 or vehicle and infected similar to that in Fig. 1a. Chromatin was isolated on Day 3 and BLIMP-1 mobilization to HIV LTR was determined using CHIP. TGF-β1 increases mobilization of BLIMP-1 to HIV LTR (a). n = NHBE ALI cultures from 4 different lungs; *significant (p < 0.05). Another set was TGF-β1 treated and infected identically, On day 6 the HDAC inhibitor vorinostat (1 μM) was added. On day 8 culture supernatants were collected and analyzed for HIV p24 (b). Total RNA was isolated and analyzed for HIV LTR using qRT-PCR (c). TGF-β1 mediated HIV transcriptional suppression can be restored by HDACi suggesting a role of histone deacetylases in TGF-β1 mediated HIV latency. n = NHBE ALI cultures from 5 different lungs; *significant (p < 0.05).