The serotonin reuptake inhibitor Fluoxetine inhibits SARS-CoV-2 in human lung tissue

Abstract To circumvent time-consuming clinical trials, testing whether existing drugs are effective inhibitors of SARS-CoV-2, has led to the discovery of Remdesivir. We decided to follow this path and screened approved medications "off-label" against SARS-CoV-2. Fluoxetine inhibited SARS-C...

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Autores principales:	Melissa Zimniak, Luisa Kirschner, Helen Hilpert, Nina Geiger, Olga Danov, Heike Oberwinkler, Maria Steinke, Katherina Sewald, Jürgen Seibel, Jochen Bodem
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/f67e6a08eef542cd9b92d04bc2ae89dd
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spelling	oai:doaj.org-article:f67e6a08eef542cd9b92d04bc2ae89dd2021-12-02T13:17:55ZThe serotonin reuptake inhibitor Fluoxetine inhibits SARS-CoV-2 in human lung tissue10.1038/s41598-021-85049-02045-2322https://doaj.org/article/f67e6a08eef542cd9b92d04bc2ae89dd2021-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-85049-0https://doaj.org/toc/2045-2322Abstract To circumvent time-consuming clinical trials, testing whether existing drugs are effective inhibitors of SARS-CoV-2, has led to the discovery of Remdesivir. We decided to follow this path and screened approved medications "off-label" against SARS-CoV-2. Fluoxetine inhibited SARS-CoV-2 at a concentration of 0.8 µg/ml significantly in these screenings, and the EC50 was determined with 387 ng/ml. Furthermore, Fluoxetine reduced viral infectivity in precision-cut human lung slices showing its activity in relevant human tissue targeted in severe infections. Fluoxetine treatment resulted in a decrease in viral protein expression. Fluoxetine is a racemate consisting of both stereoisomers, while the S-form is the dominant serotonin reuptake inhibitor. We found that both isomers show similar activity on the virus, indicating that the R-form might specifically be used for SARS-CoV-2 treatment. Fluoxetine inhibited neither Rabies virus, human respiratory syncytial virus replication nor the Human Herpesvirus 8 or Herpes simplex virus type 1 gene expression, indicating that it acts virus-specific. Moreover, since it is known that Fluoxetine inhibits cytokine release, we see the role of Fluoxetine in the treatment of SARS-CoV-2 infected patients of risk groups.Melissa ZimniakLuisa KirschnerHelen HilpertNina GeigerOlga DanovHeike OberwinklerMaria SteinkeKatherina SewaldJürgen SeibelJochen BodemNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-5 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Melissa Zimniak Luisa Kirschner Helen Hilpert Nina Geiger Olga Danov Heike Oberwinkler Maria Steinke Katherina Sewald Jürgen Seibel Jochen Bodem The serotonin reuptake inhibitor Fluoxetine inhibits SARS-CoV-2 in human lung tissue
description	Abstract To circumvent time-consuming clinical trials, testing whether existing drugs are effective inhibitors of SARS-CoV-2, has led to the discovery of Remdesivir. We decided to follow this path and screened approved medications "off-label" against SARS-CoV-2. Fluoxetine inhibited SARS-CoV-2 at a concentration of 0.8 µg/ml significantly in these screenings, and the EC50 was determined with 387 ng/ml. Furthermore, Fluoxetine reduced viral infectivity in precision-cut human lung slices showing its activity in relevant human tissue targeted in severe infections. Fluoxetine treatment resulted in a decrease in viral protein expression. Fluoxetine is a racemate consisting of both stereoisomers, while the S-form is the dominant serotonin reuptake inhibitor. We found that both isomers show similar activity on the virus, indicating that the R-form might specifically be used for SARS-CoV-2 treatment. Fluoxetine inhibited neither Rabies virus, human respiratory syncytial virus replication nor the Human Herpesvirus 8 or Herpes simplex virus type 1 gene expression, indicating that it acts virus-specific. Moreover, since it is known that Fluoxetine inhibits cytokine release, we see the role of Fluoxetine in the treatment of SARS-CoV-2 infected patients of risk groups.
format	article
author	Melissa Zimniak Luisa Kirschner Helen Hilpert Nina Geiger Olga Danov Heike Oberwinkler Maria Steinke Katherina Sewald Jürgen Seibel Jochen Bodem
author_facet	Melissa Zimniak Luisa Kirschner Helen Hilpert Nina Geiger Olga Danov Heike Oberwinkler Maria Steinke Katherina Sewald Jürgen Seibel Jochen Bodem
author_sort	Melissa Zimniak
title	The serotonin reuptake inhibitor Fluoxetine inhibits SARS-CoV-2 in human lung tissue
title_short	The serotonin reuptake inhibitor Fluoxetine inhibits SARS-CoV-2 in human lung tissue
title_full	The serotonin reuptake inhibitor Fluoxetine inhibits SARS-CoV-2 in human lung tissue
title_fullStr	The serotonin reuptake inhibitor Fluoxetine inhibits SARS-CoV-2 in human lung tissue
title_full_unstemmed	The serotonin reuptake inhibitor Fluoxetine inhibits SARS-CoV-2 in human lung tissue
title_sort	serotonin reuptake inhibitor fluoxetine inhibits sars-cov-2 in human lung tissue
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/f67e6a08eef542cd9b92d04bc2ae89dd
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The serotonin reuptake inhibitor Fluoxetine inhibits SARS-CoV-2 in human lung tissue

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