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. 2020 Jan 8;10:47. doi: 10.1038/s41598-019-56842-9

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© The Author(s) 2020

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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Summary of the anti-HBV effect of Sp1. AGI14 binds to Sp1 (see figure legend 4C), and as a result, Sp1 activity decreases, and HBV enhancer II initially increases in the presence of Sp1 and enhances HBV replication. However, it is assumed that HBV replication decreases due to decreased Sp1 activity. Moreover, when the promoter activity of Sp1 decreases, the activity of the HBV core promoter decreases, and it is expected that HBV replication will also decrease. Although the direct effect on cccDNA is unknown at this time, the possibility of reduced production of cccDNA with reduced viral replication capacity is also indicated.