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. 2017 Jun 20;7:3860. doi: 10.1038/s41598-017-04170-1

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© The Author(s) 2017

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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AAV-shRNA-1 inhibits HBV replication, transcription, and HBsAg expression in HepG2.2.15 cells. HepG2.2.15 cells were infected with AAV2-shRNA-1 at a multiplicity of infection (MOI) of 1000, 10000, and 100000. Supernatants and cells were collected separately at the indicated time points post infection. Changes of HBV DNA in supernatants (a) and cells (b), HBV RNA in cells (c), and HBsAg in supernatants (d) were monitored during a 7 day period. The inhibitory effects of different AAV-shRNAs at an MOI of 1000 on HBV DNA (e) or HBV RNA (f) were estimated by the amount of HBV DNA or HBV RNA after each treatment relative to that of the control (%). Control, PBS treatment; scrambler, vector containing the shRNA sequence not targeted to the HBV genome. P < 0.001: significant difference. Ns: the difference was not significant. Data represent the mean ± SD of three independent experiments.