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. 2021 Feb 3;11:2977. doi: 10.1038/s41598-021-82608-3

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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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Schematic draft of the dual effect of “catch-and-kill” viral inactivation at the interface between Influenza A virions and Si₃N₄: negatively charged silanol groups attract the virions at the HA methionine terminus, while highly volatile NH₃ (eluted by the Si₃N₄ surface) and NO (formed by reactions with ROS from split water) molecules penetrate the virions and damage their RNA sequence by alkaline transesterification and uracil/guanine ring disruption.