In this study, we investigated the mechanism of action (MOA) of PRSE against respiratory viruses in human-derived cells. We showed that PRSE treatment does not promote an antiviral state via expression of interferon stimulated genes (ISGs). We observed significant inhibitory effect of PRSE against respiratory syncytial virus and human metapneumovirus, which utilise clathrin-mediated endocytosis, but not human parainfluenza virus type 3, which fuses at the plasma membrane. In conclusion, we show that PRSE has broad antiviral activity and potentially perturbs virus entry via clathrin-mediated endocytosis to inhibit viral replication in vitro.
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