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. 2017 Nov 24;7:16278. doi: 10.1038/s41598-017-16446-7

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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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The antiviral effects of ICAC against EV71 were disrupted by BSO administration. Infected (100 TCID₅₀ of EV71) Vero cells, treated with 100 µM ICAC, exposed to various concentrations of BSO (0~500 µM). Uninfected cells were used as the control group. Vero cells infected with 100 TCID₅₀ of EV71 alone were used as the model group. Cell viability was detected using the MTS cell proliferation assay kit at 48 hpi. The viability of the control group was set as 100% (n = 6). Asterisks indicate that the data significantly differ from the ICAC group at the P < 0.05 level according to one-way analysis of variance.