Abstract
Heparin is an anticoagulant medicine that prevents the formation of harmful blood clots in the vessels. Following the outbreak of the novel coronavirus disease 2019 (COVID-19), heparin has helped to improve the health of affected patients beyond its anticoagulant effects. The potential antiviral activity of heparin has attracted speculation due to its highly sulfated profile, which allows it to have a high binding affinity to a wide range of viral components. Heparin’s successful binding to the ZIKA virus, human immunodeficiency virus, as well as the SARS CoV and MERS CoV spike proteins have demonstrated its potential to inhibit the entry of SARS-CoV-2 into the body. A high degree of sequence homology also enables heparin to have inhibitory binding potential on viral components. The SARS-CoV-2 virus exhibits significant differences in its spike glycoprotein (SGP) sequence compared to other coronaviruses. The SGP sequence in SARS-CoV-2 contains additional potential glycosaminoglycan (GAG) binding domains that may drive differences in the attachment and entry process of the virus. Findings from unbiased computational ligand docking simulations, pseudotyped spike protein experiments, and cell to cell fusion assays have also opened possibilities to investigate the antiviral properties of heparin in clinical trials
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