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. 2018 Nov 16;8:16956. doi: 10.1038/s41598-018-34732-w

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© The Author(s) 2018

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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Carbenoxolone inhibits VACV replication in a gap junction-independent manner. Cells ((A) HaCaT and (C) N2a) were untreated or treated with different concentrations of CBX and then infected with VACV-A5L-EGFP (MOI = 0.1). Virus levels were determined by fluorescence. Results of untreated cells and cells treated with 30 µM CBX were analysed by t test, *** denotes p < 0.05. Cell viability ((B) HaCaT and (D) N2a) was defined by CellTiter-Blue ® assay. Non-treated cells were designated as 100% viability. IC₅₀ and CC₅₀ values (48 h p.i.) are noted. Experiments are representative of two independent replicates performed in triplicate. Error bars = standard deviation.