tetano
Editor, Senior Moderator
Nature
. 2020 Jul 22.
doi: 10.1038/s41586-020-2575-3. Online ahead of print.
Chloroquine does not inhibit infection of human lung cells with SARS-CoV-2
Markus Hoffmann[SUP] 1 2 [/SUP], Kirstin M?sbauer[SUP] 3 4 [/SUP], Heike Hofmann-Winkler[SUP] 5 [/SUP], Artur Kaul[SUP] 5 [/SUP], Hannah Kleine-Weber[SUP] 5 6 [/SUP], Nadine Kr?ger[SUP] 5 [/SUP], Nils C Gassen[SUP] 7 [/SUP], Marcel A M?ller[SUP] 3 4 8 [/SUP], Christian Drosten[SUP] 3 4 [/SUP], Stefan P?hlmann[SUP] 9 10 [/SUP]
Affiliations
Abstract
The COVID-19 pandemic, which is caused by the novel coronavirus SARS-CoV-2, has been associated with more than 470,000 fatal cases worldwide. In order to develop antiviral interventions quickly, drugs used for treatment of unrelated diseases are currently being repurposed to combat COVID-19. Chloroquine is a anti-malaria drug that is frequently employed for COVID-19 treatment since it inhibits SARS-CoV-2 spread in the kidney-derived cell line Vero[SUP]1-3[/SUP]. Here, we show that engineered expression of TMPRSS2, a cellular protease that activates SARS-CoV-2 for entry into lung cells[SUP]4[/SUP], renders SARS-CoV-2 infection of Vero cells insensitive to chloroquine. Moreover, we report that chloroquine does not block SARS-CoV-2 infection of the TMPRSS2-positive lung cell line Calu-3. These results indicate that chloroquine targets a pathway for viral activation that is not operative in lung cells and is unlikely to protect against SARS-CoV-2 spread in and between patients.
. 2020 Jul 22.
doi: 10.1038/s41586-020-2575-3. Online ahead of print.
Chloroquine does not inhibit infection of human lung cells with SARS-CoV-2
Markus Hoffmann[SUP] 1 2 [/SUP], Kirstin M?sbauer[SUP] 3 4 [/SUP], Heike Hofmann-Winkler[SUP] 5 [/SUP], Artur Kaul[SUP] 5 [/SUP], Hannah Kleine-Weber[SUP] 5 6 [/SUP], Nadine Kr?ger[SUP] 5 [/SUP], Nils C Gassen[SUP] 7 [/SUP], Marcel A M?ller[SUP] 3 4 8 [/SUP], Christian Drosten[SUP] 3 4 [/SUP], Stefan P?hlmann[SUP] 9 10 [/SUP]
Affiliations
- PMID: 32698190
- DOI: 10.1038/s41586-020-2575-3
Abstract
The COVID-19 pandemic, which is caused by the novel coronavirus SARS-CoV-2, has been associated with more than 470,000 fatal cases worldwide. In order to develop antiviral interventions quickly, drugs used for treatment of unrelated diseases are currently being repurposed to combat COVID-19. Chloroquine is a anti-malaria drug that is frequently employed for COVID-19 treatment since it inhibits SARS-CoV-2 spread in the kidney-derived cell line Vero[SUP]1-3[/SUP]. Here, we show that engineered expression of TMPRSS2, a cellular protease that activates SARS-CoV-2 for entry into lung cells[SUP]4[/SUP], renders SARS-CoV-2 infection of Vero cells insensitive to chloroquine. Moreover, we report that chloroquine does not block SARS-CoV-2 infection of the TMPRSS2-positive lung cell line Calu-3. These results indicate that chloroquine targets a pathway for viral activation that is not operative in lung cells and is unlikely to protect against SARS-CoV-2 spread in and between patients.