How does Heparan Sulfate and COVID-19 Work?: An Overview

Abstract

Globally, the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) had infected over 3 million individuals and claimed many lives producing a global epidemic that necessitates the rapid development of therapeutic solutions. The ideal technique for quickly deploying well-characterized medicines against novel infections is known as drug repurposing. Several repurposable medicines are currently being tested to see if they may be used to treat COVID-19. Heparin, which is commonly utilized to reduce thrombotic events associated with COVID-19-induced disease, is one such promising drug. Heparansulphate is prevalently expressed in mammalian tissues. CoV-2 requires the helping cofactor heparansulphate (HS) on the cell surface: knocking down genes related in HS formation or treating cells with an HS mimic both prevent spike-mediated viral entrance. Heparin/HS binds directly to spike and promotes viral entrance by facilitating the attachment of spike-bearing viral particles to the cell surface. As documented with cell surface-bound heparansulphate, heparin binding to the open conformation of the spike structurally supports the state and may enhance ACE2 binding. Thus, heparansulphate could potentially be utilised to prevent SARS-CoV-2 transmission, based on available datas also consumption of heparansulphate during SARS-CoV-2 cellular entrance may play a role in the thrombotic events associated with COVID-19 infection. Furthermore, this study provides the findings on the mechanism(s) by which heparansulphate could slow the progression of SARS-CoV-2 infection.
 Keywords: COVID-19, HeparanSulphate, Spike Protiens