Fig. 6: C10 suppresses viral translation and modulates host responses.

a Polysome profiling of SARS-CoV-2 trVLP infected A549-ACE2 cells treated with C10 (20 µM or 40 µM) or DMSO for 8 h, respectively. FF, free fraction. b Left panel: Ratio of SARS-CoV-2 spike mRNA relative to host HPRT1 in lysates of A549-ACE2 cells treated with C10 (20 µM or 40 µM) or DMSO and infected with SARS-CoV-2 trVLP for 8 h, respectively, prior to polysome fractionation. Right panel: Ratio of SARS-CoV-2 trVLP spike mRNA relative to host HPRT1 in the free fraction or heavy polysomal fraction of lysates of A549-ACE2 cells treated with C10 (20 µM or 40 µM) or DMSO and infected with SARS-CoV-2 trVLP for 8 h, respectively, after polysome fractionation. Data are presented as mean ± SD from three independent replicates. Statistical significance was analyzed by two-sided unpaired t-test. c, d Quantification of SARS-CoV-2 spike expression by qPCR (c) and western blotting (d) in SARS-CoV-2 trVLP infected A549-ACE2 cells treated with 20 µM C10. Data are presented as mean ± SD from three independent replicates. Statistical significance was analyzed by two-sided unpaired t-test. e C10 inhibition of SARS-CoV-2 trVLP replication induces ISG expression in A549-ACE2 cells. Cells were mock-infected or infected with SARS-CoV-2 trVLP, pre-treated for 1 h with DMSO, C10 (20 µM), or remdesivir (1 µM), respectively; IFNB1 protein (10 nM) served as a positive control. Host and viral transcripts were quantified by qPCR 24 h post-infection. Data are presented as mean ± SD from three independent replicates. Source data are provided as a Source Data file.