Could Endogenous Glucocorticoids Influence SARS-CoV-2 Infectivity?

Could Endogenous Glucocorticoids Influence SARS-CoV-2 Infectivity?

Blog Article

Endogenous glucocorticoids and their synthetic analogues, such as dexamethasone, stimulate receptor-mediated signal transduction mechanisms on target cells.Some of these mechanisms result in beneficial outcomes whereas others are deleterious in the settings of pathogen infections and immunological ANTIOXIDANT 7 disorders.Here, we review recent studies by several groups, including our group, showing that glucocorticoids can directly interact with protein components on SARS-CoV-2, the causative agent of COVID-19.We postulate an antiviral defence mechanism by which endogenous glucocorticoids (e.

g., cortisol produced in response to SARS-CoV-2 infection) can bind to multiple sites on SARS-CoV-2 surface APPLE SAUCE ORG protein, Spike, inducing conformational alterations in Spike subunit 1 (S1) that inhibit SARS-CoV-2 interaction with the host SARS-CoV-2 receptor, ACE2.We suggest that glucocorticoids-mediated inhibition of S1 interaction with ACE2 may, consequently, affect SARS-CoV-2 infectivity.Further, glucocorticoids interactions with Spike could protect against a broad spectrum of coronaviruses and their variants that utilize Spike for infection of the host.

These notions may be useful for the design of new antivirals for coronavirus diseases.