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Heme oxygenase-1 inducer hemin does not inhibit SARS-CoV-2 virus infection

Antiviral agents with different mechanisms of action could induce synergistic effects against SARS-CoV-2 infection. Some reports suggest the therapeutic potential of the heme oxygenase-1 (HO-1) enzyme against virus infection. Given that hemin is a natural inducer of the HO-1 gene, the aim of this st...

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Autores principales: Maestro, Sheila, Córdoba, Karol M., Olague, Cristina, Argemi, Josepmaria, Ávila, Matías A., González-Aseguinolaza, Gloria, Smerdou, Cristian, Fontanellas, Antonio
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Author(s). Published by Elsevier Masson SAS. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7881701/
https://www.ncbi.nlm.nih.gov/pubmed/33761605
http://dx.doi.org/10.1016/j.biopha.2021.111384
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author Maestro, Sheila
Córdoba, Karol M.
Olague, Cristina
Argemi, Josepmaria
Ávila, Matías A.
González-Aseguinolaza, Gloria
Smerdou, Cristian
Fontanellas, Antonio
author_facet Maestro, Sheila
Córdoba, Karol M.
Olague, Cristina
Argemi, Josepmaria
Ávila, Matías A.
González-Aseguinolaza, Gloria
Smerdou, Cristian
Fontanellas, Antonio
author_sort Maestro, Sheila
collection PubMed
description Antiviral agents with different mechanisms of action could induce synergistic effects against SARS-CoV-2 infection. Some reports suggest the therapeutic potential of the heme oxygenase-1 (HO-1) enzyme against virus infection. Given that hemin is a natural inducer of the HO-1 gene, the aim of this study was to develop an in vitro assay to analyze the antiviral potency of hemin against SARS-CoV-2 infection. A SARS-CoV-2 infectivity assay was conducted in Vero-E6 and Calu-3 epithelial cell lines. The antiviral effect of hemin, and chloroquine as a control, against SARS-CoV-2 virus infection was quantified by RT-qPCR using specific oligonucleotides for the N gene. Chloroquine induced a marked reduction of viral genome copies in kidney epithelial Vero-E6 cells but not in lung cancer Calu-3 cells. Hemin administration to the culture medium induced a high induction in the expression of the HO-1 gene that was stronger in Vero-E6 macaque-derived cells than in the human Calu-3 cell line. However, hemin treatment did not modify SARS-CoV-2 replication, as measured by viral genome quantification 48 h post-infection for Vero-E6 and 72 h post-infection for the Calu-3 lineages. In conclusion, although exposure to hemin induced strong HO-1 up-regulation, this effect was unable to inhibit or delay the progression of SARS-CoV-2 infection in two epithelial cell lines susceptible to infection.
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spelling pubmed-78817012021-02-16 Heme oxygenase-1 inducer hemin does not inhibit SARS-CoV-2 virus infection Maestro, Sheila Córdoba, Karol M. Olague, Cristina Argemi, Josepmaria Ávila, Matías A. González-Aseguinolaza, Gloria Smerdou, Cristian Fontanellas, Antonio Biomed Pharmacother Short Communication Antiviral agents with different mechanisms of action could induce synergistic effects against SARS-CoV-2 infection. Some reports suggest the therapeutic potential of the heme oxygenase-1 (HO-1) enzyme against virus infection. Given that hemin is a natural inducer of the HO-1 gene, the aim of this study was to develop an in vitro assay to analyze the antiviral potency of hemin against SARS-CoV-2 infection. A SARS-CoV-2 infectivity assay was conducted in Vero-E6 and Calu-3 epithelial cell lines. The antiviral effect of hemin, and chloroquine as a control, against SARS-CoV-2 virus infection was quantified by RT-qPCR using specific oligonucleotides for the N gene. Chloroquine induced a marked reduction of viral genome copies in kidney epithelial Vero-E6 cells but not in lung cancer Calu-3 cells. Hemin administration to the culture medium induced a high induction in the expression of the HO-1 gene that was stronger in Vero-E6 macaque-derived cells than in the human Calu-3 cell line. However, hemin treatment did not modify SARS-CoV-2 replication, as measured by viral genome quantification 48 h post-infection for Vero-E6 and 72 h post-infection for the Calu-3 lineages. In conclusion, although exposure to hemin induced strong HO-1 up-regulation, this effect was unable to inhibit or delay the progression of SARS-CoV-2 infection in two epithelial cell lines susceptible to infection. The Author(s). Published by Elsevier Masson SAS. 2021-05 2021-02-13 /pmc/articles/PMC7881701/ /pubmed/33761605 http://dx.doi.org/10.1016/j.biopha.2021.111384 Text en © 2021 The Authors Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.
spellingShingle Short Communication
Maestro, Sheila
Córdoba, Karol M.
Olague, Cristina
Argemi, Josepmaria
Ávila, Matías A.
González-Aseguinolaza, Gloria
Smerdou, Cristian
Fontanellas, Antonio
Heme oxygenase-1 inducer hemin does not inhibit SARS-CoV-2 virus infection
title Heme oxygenase-1 inducer hemin does not inhibit SARS-CoV-2 virus infection
title_full Heme oxygenase-1 inducer hemin does not inhibit SARS-CoV-2 virus infection
title_fullStr Heme oxygenase-1 inducer hemin does not inhibit SARS-CoV-2 virus infection
title_full_unstemmed Heme oxygenase-1 inducer hemin does not inhibit SARS-CoV-2 virus infection
title_short Heme oxygenase-1 inducer hemin does not inhibit SARS-CoV-2 virus infection
title_sort heme oxygenase-1 inducer hemin does not inhibit sars-cov-2 virus infection
topic Short Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7881701/
https://www.ncbi.nlm.nih.gov/pubmed/33761605
http://dx.doi.org/10.1016/j.biopha.2021.111384
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