AI Article Synopsis
- SARS-CoV-2 uses ACE2 for cell entry but may also bind to heparan sulfates, which are potential attachment receptors.
- Recent studies have shown that the spike protein of SARS-CoV-2 has an affinity for heparan sulfates and that this binding can be inhibited using heparin or heparinase.
- The research explored various sulfated and sulfonated compounds that block interaction with heparan sulfates, revealing that certain nanoparticles and sulfonated cyclodextrins can effectively inhibit SARS-CoV-2 at low concentrations, but this inhibition is reversible.
Article Abstract
Severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) depends on angiotensin converting enzyme 2 (ACE2) for cellular entry, but it might also rely on attachment receptors such as heparan sulfates. Several groups have recently demonstrated an affinity of the SARS-CoV2 spike protein for heparan sulfates and a reduced binding to cells in the presence of heparin or heparinase treatment. Here, we investigated the inhibitory activity of several sulfated and sulfonated molecules, which prevent interaction with heparan sulfates, against vesicular stomatitis virus (VSV)-pseudotyped-SARS-CoV-2 and the authentic SARS-CoV-2. Sulfonated cyclodextrins and nanoparticles that have recently shown broad-spectrum non-toxic virucidal activity against many heparan sulfates binding viruses showed inhibitory activity in the micromolar and nanomolar ranges, respectively. In stark contrast with the mechanisms that these compounds present for these other viruses, the inhibition against SARS-CoV-2 was found to be simply reversible.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7760145 | PMC |
| http://dx.doi.org/10.3390/microorganisms8121894 | DOI Listing |
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