TMPRSS2的工程化表达（一种激活SARS-CoV-2进入肺细胞的细胞蛋白酶）可使SARS-CoV-2感染Vero细胞对氯喹不敏感。此外，研究人员发现，氯喹不会阻止TMPRSS2阳性肺细胞株Calu-3的SARS-CoV-2感染。这些结果表明，氯喹靶向病毒激活的途径，但该途径在肺细胞中不起作用，并且不太可能防止SARS-CoV-2在患者体内和患者之间的传播。

 为了快速开发抗病毒干预措施，目前正在将用于治疗无关疾病的药物重新用于对抗COVID-19。氯喹是一种抗疟疾药物，经常用于COVID-19治疗，因为它能够抑制SARS-CoV-2在肾源性细胞系Vero中的传播。

附：英文原文

Title: Chloroquine does not inhibit infection of human lung cells with SARS-CoV-2

Author: Markus Hoffmann, Kirstin Msbauer, Heike Hofmann-Winkler, Artur Kaul, Hannah Kleine-Weber, Nadine Krger, Nils C. Gassen, Marcel A. Mller, Christian Drosten, Stefan Phlmann

Issue&Volume: 2020-07-22

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 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.

DOI: 10.1038/s41586-020-2575-3

Source: https://www.nature.com/articles/s41586-020-2575-3