@article{GeigerKoenigOberwinkleretal.2022,
  author    = {Geiger, Nina and K{\"o}nig, Eva-Maria and Oberwinkler, Heike and Roll, Valeria and Diesendorf, Viktoria and F{\"a}hr, Sofie and Obernolte, Helena and Sewald, Katherina and Wronski, Sabine and Steinke, Maria and Bodem, Jochen},
  title     = {Acetylsalicylic acid and salicylic acid inhibit SARS-CoV-2 replication in precision-cut lung slices},
  series = {Vaccines},
  volume    = {10},
  journal   = {Vaccines},
  number    = {10},
  issn      = {2076-393X},
  doi       = {10.3390/vaccines10101619},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-289885},
  year      = {2022},
  abstract  = {Aspirin, with its active compound acetylsalicylic acid (ASA), shows antiviral activity against rhino- and influenza viruses at high concentrations. We sought to investigate whether ASA and its metabolite salicylic acid (SA) inhibit SARS-CoV-2 since it might use similar pathways to influenza viruses. The compound-treated cells were infected with SARS-CoV-2. Viral replication was analysed by RTqPCR. The compounds suppressed SARS-CoV-2 replication in cell culture cells and a patient-near replication system using human precision-cut lung slices by two orders of magnitude. While the compounds did not interfere with viral entry, it led to lower viral RNA expression after 24 h, indicating that post-entry pathways were inhibited by the compounds.},
  language  = {en}
}
@article{ZimniakKirschnerHilpertetal.2021,
  author    = {Zimniak, Melissa and Kirschner, Luisa and Hilpert, Helen and Geiger, Nina and Danov, Olga and Oberwinkler, Heike and Steinke, Maria and Sewald, Katherina and Seibel, J{\"u}rgen and Bodem, Jochen},
  title     = {The serotonin reuptake inhibitor Fluoxetine inhibits SARS-CoV-2 in human lung tissue},
  series = {Scientific Reports},
  volume    = {11},
  journal   = {Scientific Reports},
  doi       = {10.1038/s41598-021-85049-0},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-259820},
  pages     = {5890},
  year      = {2021},
  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 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.},
  language  = {en}
}