Yingying Cong

We further evaluated the inhibition effects of model compound 2a on the replication of the live SARS-CoV-2 virus. To this aim, we first perform a cytotoxic assay of 2a in A549-hACE2 cells to determine the maximal non-toxic concentration of it that could be used in cells by MTT, and we did not observe the obvious cytotoxicity at a concentration up to ∼2 μM ( Figure 8 A). We further investigate the antiviral effect of 2a at concentrations from 0.125 to 2 μM, with a serial dilution factor of 2.

Abstract Influenza A virus (IAV) enters host cells via endocytosis, and fusion of the viral particles (VPs) at endosomes releases the viral ribonucleoproteins (vRNPs) into the cytoplasm. This uncoating step that is vital for IAV infection remains to be fully understood. The aggresome processing machinery (APM) plays a relevant but not essential role in this.

Introduction Pyrimidine nucleotides are building blocks of DNA and RNA, and are essential for all living organisms. There are two mechanisms for pyrimidine generation: the salvage and de novo biosynthesis pathways (Figure S1). Generally, the de novo pathway is up-regulated in rapidly proliferating cancer cells due to continuous demand for nucleic acids,1 whereas resting cells are typically dependent on the pyrimidine salvage pathway (e. g.