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Updated: May 12, 2026

Early Viral Entry Assays for the Identification and Evaluation of Antiviral Compounds
Published on: October 29, 2015
Polyphenol rich sugarcane extract restricts select respiratory viruses depending on their mode of entry
Caolingzhi Tang1, Matthew Flavel2, Sarah L Londrigan1
1Department of Microbiology and Immunology, The University of Melbourne at the Peter Doherty Institute for Infection and Immunity, 792 Elizabeth Street, Melbourne, VIC, 3000, Australia.
Abstract:
We previously showed that Polyphenol rich sugarcane extract (PRSE) displayed significant inhibitory effect against influenza A virus (IAV). 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 subsequently investigated any potential perturbation on the viral entry process and observed that PRSE treatment did not affect caveolin-mediated endocytosis but led to a significant attenuation in clathrin-mediated endocytosis. We confirmed this inhibitory effect on IAV entry, as infection was unaffected by PRSE when IAV fusion was induced at the plasma membrane, instead of endosomal membranes. Based on these findings 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.
Insights
Polyphenol-rich sugarcane extract (PRSE) inhibits influenza A virus (IAV) by blocking clathrin-mediated endocytosis. This extract shows broad antiviral activity against respiratory viruses that use this entry pathway.
Area of Science:
- Virology
- Cell Biology
- Natural Product Therapeutics
Background:
- Polyphenol-rich sugarcane extract (PRSE) previously demonstrated significant inhibitory effects against influenza A virus (IAV).
- Understanding the precise mechanism of action (MOA) of PRSE against respiratory viruses is crucial for developing novel antiviral strategies.
Purpose of the Study:
- To elucidate the MOA of PRSE against respiratory viruses in human-derived cells.
- To determine if PRSE induces an antiviral state or interferes with viral entry pathways.
Main Methods:
- PRSE treatment effects on interferon-stimulated genes (ISGs) were assessed.
- Viral entry mechanisms, including caveolin-mediated and clathrin-mediated endocytosis, were investigated.
- IAV entry was studied under conditions of plasma membrane fusion versus endosomal fusion.
Main Results:
- PRSE did not induce an antiviral state via ISG expression.
- PRSE significantly attenuated clathrin-mediated endocytosis but did not affect caveolin-mediated endocytosis.
- PRSE inhibited IAV entry when fusion occurred in endosomes, but not at the plasma membrane.
- PRSE showed inhibitory effects against respiratory syncytial virus and human metapneumovirus, but not human parainfluenza virus type 3.
Conclusions:
- PRSE exhibits broad-spectrum antiviral activity against respiratory viruses.
- PRSE's MOA involves the perturbation of clathrin-mediated endocytosis, a key viral entry pathway.
- PRSE demonstrates potential as an in vitro antiviral agent by inhibiting viral replication through interference with cellular entry mechanisms.
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