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Heparin may stop SARS-CoV-2 infecting host cells

Date: 26 May 2020 Tags: Miscellaneous

Issue

The researchers have found that incubating the cells with unfractionated heparin, stopped the spike protein of the virus binding to them.

 

Background

The spike protein is the main structure that SARS-CoV-2 uses to bind to ACE2 receptors expressed on target cells, before infecting them and potentially causing coronavirus disease 2019 (COVID-19).

 

Details

  • On binding to ACE2, the spike protein undergoes host cell proteolytic cleavage into two subunits: S1, which contains the receptor-binding domain (RBD) and S2, which enables fusion with the host cell membrane and viral entry.

  • They found that an intact recombinant form of the viral spike protein containing both S1 and S2 (S1S2), but not the S1 domain alone, binds strongly to RT4 cells in a temperature-dependent manner.

  • Most cell types only express quite low levels of ACE2, suggesting that the spike protein might also interact with other receptor sites to gain viral entry.

  • Certain viruses such as herpes simplex are already known to bind with host glycosamin oglycans called heparan sulfates.

  • In addition, a study suggested that the soluble glycosaminoglycan heparin can inhibit the entry of SARS CoV-2 into “Vero” cells, a cell line derived from monkey kidney epithelia.

  • The team reports that unfractionated heparin (UFH) completely inhibited the binding of S1S2 to RT4 cells. Treating the cells with two low molecular weight heparins (LMWHs) that are already in clinical use also inhibited the binding, but only partially and not as strongly.

  • The experiment did not result in any significant reduction in the binding of RT4 cells, suggesting that heparan sulfates do not play any significant role in the attachment of SARS-CoV-2 spike protein to host cells.