TY  - JOUR
A1  - Zimniak, Melissa
A1  - Kirschner, Luisa
A1  - Hilpert, Helen
A1  - Geiger, Nina
A1  - Danov, Olga
A1  - Oberwinkler, Heike
A1  - Steinke, Maria
A1  - Sewald, Katherina
A1  - Seibel, Jürgen
A1  - Bodem, Jochen
T1  - The serotonin reuptake inhibitor Fluoxetine inhibits SARS-CoV-2 in human lung tissue
JF  - Scientific Reports
N2  - 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 mu g/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.
KW  - SARS-CoV-2
KW  - viral epidemiology
KW  - viral infection
Y1  - 2021
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-259820
VL  - 11
ER  -