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. 2021 Jan 26;7:24. doi: 10.1038/s41420-020-00379-8

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© The Author(s) 2021

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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Fig. 2 — a JEG-3 and HTR-8 infected with 1.0 MOI MRV or PRV showing significant increase in caspase 3/7 activity compared to uninfected vehicle cells (left panel). Similarly, ZIKV infection with 1.0 MOI MRV or PRV also showed increased percentage apoptotic nuclei compared to uninfected vehicle cells (right). Similarly, ZIKV infection with 0.1 MOI r-MRV to placental trophoblast also induces apoptosis as evidenced by an increase in caspase 3/7 activity and percent apoptotic nuclei and in JEG-3 (b), JAR (c), and HTR-8 (d) cells compared to uninfected vehicle cells. Each value presents mean ± SEM of biological replicates (n = 4) for caspase 3/7 activity and (n = 3) for percentage apoptotic nuclear morphology, *P < 0.05 compared to uninfected vehicle cells; statistical comparison by Student’s t-test.