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© A-M. Pais-Correia, M-I. Thoulouze, A. Alcover, A. Gessain
Mise en évidence de structures de type "biofilm ", formées par le rétrovirus HTLV-1 générés par des cellules infectées (cellules du haut), qui ont été transmis à un autre lymphocyte (cellule du bas). Micrographie en microscopie électronique à balayage. Image colorisée.
Publication : iScience

The FDA-approved drug Auranofin has a dual inhibitory effect on SARS-CoV-2 entry and NF-κB signaling.

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in iScience - 21 Oct 2022

Laplantine E, Chable-Bessia C, Oudin A, Swain J, Soria A, Merida P, Gourdelier M, Mestiri S, Besseghe I, Bremaud E, Neyret A, Lyonnais S, Favard C, Benaroch P, Hubert M, Schwartz O, Guerin M, Danckaert A, Del Nery E, Muriaux D, Weil R,

Link to Pubmed [PMID] – 36093378

Link to DOI – 10506610.1016/j.isci.2022.105066

iScience 2022 Oct; 25(10): 105066

Patients with severe COVID-19 show an altered immune response that fails to control the viral spread and suffer from exacerbated inflammatory response, which eventually can lead to death. A major challenge is to develop an effective treatment for COVID-19. NF-κB is a major player in innate immunity and inflammatory process. By a high-throughput screening approach, we identified FDA-approved compounds that inhibit the NF-κB pathway and thus dampen inflammation. Among these, we show that Auranofin prevents post-translational modifications of NF-κB effectors and their recruitment into activating complexes in response to SARS-CoV-2 infection or cytokine stimulation. In addition, we demonstrate that Auranofin counteracts several steps of SARS-CoV-2 infection. First, it inhibits a raft-dependent endocytic pathway involved in SARS-CoV-2 entry into host cells; Second, Auranofin alters the ACE2 mobility at the plasma membrane. Overall, Auranofin should prevent SARS-CoV-2 infection and inflammatory damages, offering new opportunities as a repurposable drug candidate to treat COVID-19.

https://pubmed.ncbi.nlm.nih.gov/36093378