PMC:7435837 / 46831-48059
Annnotations
{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7435837","sourcedb":"PMC","sourceid":"7435837","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7435837","text":"Figure 2 Potential targets for drug therapy. (A). The virus spike proteins interact with ACE-2 receptors and this provides the route of entry of the virus into the host cell. 1. Drugs such as arbidol interfere with the binding of spike proteins with ACE-2 receptor. 2. Priming of the spike protein to enhance its affinity for ACE-2 receptors is hampered by, for example, camostat. 3. Virus-host membrane fusion could be prevented by drugs such as chloroquine. (B). The successful fusion of the virus and host membrane is achieved. (C). The coronavirus sheds its RNA which can then be translated to polypeptides. The polypeptides as cleaved by the enzyme, 3-chymotrypsin protease to render non-structural proteins. This proteolysis step, 4, can be inhibited by, for example, lopinavir. Drug target 5, prohibits the further conversion of non-structural to structural proteins by RNA-dependent polymerase enzymes. Remdesivir is a prime example of an inhibitor of target 5. (D). Virus assembly has been completed and the virus is expelled from the host cell. The virus can then be intercepted by dendritic cells or other immune factors such as interferons (not discussed) or restart the replication cycle. Figure adapted from 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