Fig. 1: Chloroquine does not block infection of human lung cells with SARS-CoV-2. | Nature

Fig. 1: Chloroquine does not block infection of human lung cells with SARS-CoV-2.

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

Fig. 1

a, Vero, TMPRSS2-expressing Vero and Calu-3 cells were preincubated for 2 h with the respective inhibitors (0 μM, 0.01 μM, 0.1 μM, 1 μM, 10 μM or 100 μM) and then inoculated with replication-defective vesicular stomatitis virus reporter particles bearing the S protein. Top, the transduction efficiency of the virus was assessed. Bottom, cells were not inoculated with virus particles but cell viability after drug treatment was instead assessed at the same time as transduction was quantified. Transduction efficiency was quantified by measuring virus-encoded luciferase activity in cell lysates. Cell viability was measured using the CellTiter-Glo assay. Data are mean ± s.e.m. of three biological replicates, each of which consisted of quadruplicate samples. Data were normalized as the relative entry efficiency or cell viability of inhibitor-treated cells compared with those of untreated cells (set to 100%). The calculated 50% inhibitory concentration (IC50) values are summarized in Table 1. b, Untreated or chloroquine-preincubated Vero and Calu-3 cells were inoculated with SARS-CoV-2 Munich isolate (patient isolate 929, BetaCoV/Munich/BavPat1/2020|EPI_ISL_406862) at a multiplicity of infection (MOI) of 0.001. After inoculation for 24 h, viral RNA was isolated from the culture supernatant (extracellular virus) (dark blue) and the infected cells (intracellular virus) (light blue), and SARS-CoV-2 genome equivalents (GE) were determined by quantitative PCR with reverse transcription. Data are mean ± s.e.m. of three biological replicates, each of which consisted of single samples. c, The experiment was conducted as described in b, but the number of infectious SARS-CoV-2 particles in culture supernatants was determined by plaque titration using Vero E6 cells. PFU, plaque-forming units. Statistical significance was analysed by two-way analysis of variance (ANOVA) with Dunnett’s post hoc test. NS, not significant (P > 0.05); *P ≤ 0.05; **P ≤ 0.01; ***P ≤ 0.001. P values (from left to right) are as follows. a, Entry efficiency (camostat mesylate/chloroquine/hydroxychloroquine), Vero (0.9999/0.8587/0.9997, 0.9842/0.9846/0.3904, 0.6860/0.0991/0.0223, 0.9968/0.0001/0.0001, 0.9997/0.0001/0.0001), TMPRSS2-expressing Vero (0.9999/0.9968/0.9795, 0.1251/0.9962/0.9998, 0.0004/0.9997/0.9999, 0.0001/0.9967/0.9982, 0.0001/0.9981/0.9986; Calu-3 (0.9900/0.9999/0.9986, 0.0003/0.9999/0.9983, 0.0001/0.9988/0.9929, 0.0001/0.1291/0.9938, 0.0001/0.0005/0.0045); cell viability (camostat mesylate/chloroquine/hydroxychloroquine), Vero (0.9273/0.9999/0.9999, 0.9999/0.8710/0.9642, 0.9999/0.9996/0.9999, 0.9999/0.8958/0.4818, 0.9998/0.0838/0.0161), TMPRSS2-expressing Vero (0.9998/0.9999/0.9959, 0.9811/0.9985/0.9362, 0.9998/0.9985/0.9997, 0.9997/0.8835/0.9998, 0.9999/0.0315/0.1422), Calu-3 (0.9986/0.9999/0.9999, 0.9999/0.9997/0.9999, 0.9986/0.9999/0.8134, 0.9924/0.9275/0.7125, 0.9983/0.0492/0.0002). b, (extracellular/intracellular), Vero (0.6844/0.6989, 0.0121/0.0002, 0.0002/0.0001), Calu-3 (0.9434/0.8800, 0.9999/0.8830, 0.0517/0.3924). c, (extracellular/intracellular), Vero (0.9561, 0.0001, 0.0001), Calu-3 (0.1184, 0.9997, 0.0987).

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