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 Vero1–3. Here, we show that engineered expression of TMPRSS2, a cellular protease that activates SARS-CoV-2 for entry into lung cells4, 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.
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Hoffmann, M., Mösbauer, K., Hofmann-Winkler, H. et al. Chloroquine does not inhibit infection of human lung cells with SARS-CoV-2. Nature (2020). https://doi.org/10.1038/s41586-020-2575-3
Response to: ‘Hydroxychloroquine ineffective for COVID-19 prophylaxis in lupus and rheumatoid arthritis’ by Singer et al
Annals of the Rheumatic Diseases (2020)