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editorial

. 2022 Jan 17;29(2):263–265. doi: 10.1038/s41418-021-00909-6

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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. 1 — The intracellular replication of SARS-CoV-2 is mediated by the viral RNA-dependent RNA polymerase (NSP12). The incorporation of remdesivir terminates the assemble of viral genomes. However, the efficacy of remdesivir could be compromised by RNA proofreading complex (NSP10/NSP14), Blocking NSP14 activity by solfacone dramatically lowered the IC50 of remdesivir. The continuous intracellular virus replication would induce typical cellular senescence with the induction of anti-apoptotic Bcl-2 family and PI3K signaling cascade. Senolytics, such as fisetin and quercetin, could help to clear infected cells and resolve inflammation in COVID-19 infections.