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. 2022 Sep 21;7:109. doi: 10.1038/s41541-022-00536-3

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© The Author(s) 2022

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. 1 — a Schematic representation of the RVax-1 S, M, and L segments, which encode a deletion at nt. 21–384 in the M-segment, and 566 silent mutations throughout the N, M, and L ORFs. Locations of individual silent mutations are labeled in red lines, which are found as a cluster every 50 nt. b Plaque phenotypes of rMP-12 and RVax-1 in Vero cells at 4 dpi. The graph represents the means ± standard deviations of relative diameter lengths from 20 randomly selected plaques. Unpaired t-test was used for the comparison of two groups (t = 7.319, df = 38). Vero cells (c) or MRC-5 cells (d) were infected with MP-12 vaccine lot-7-2-88, rMP-12 or RVax-1 in Vero cells at MOI 0.01. Virus replication kinetics at 35 °C are shown. Means ± standard deviations of triplicate wells are shown.