Changes in cortisol secretion and the role of the glucocorticoid receptor in the development of the immune response in patients with SARS-CoV-2 infection

With the outbreak of the COVID-19 pandemic, the scientific community has directed its attention towards studying the impact of the causative agent, SARS-CoV-2, on the endocrine system. It has been proven that the virus exhibits organotropism towards the cortex of the adrenal glands, causing tissue damage and hormonal dysfunction. The aim of this exposition is to address the question of whether SARS-CoV-2 causes disruptions in the hormonal regulation of glucocorticoid hormones. Based on a thorough review of the current literature, it is suggested that the virus could potentially directly damage the hypothalamus, leading to a disruption in the regulation of the hypothalamic-pituitary-adrenal axis. The decrease in cortisol secretion is a secondary effect. As a result, there is a loss of stress-induced cortisol elevation due to the inflammatory process and an increased risk of adrenal crisis. On the other hand, inflammatory cytokines synthesized during the inflammatory process could stimulate cortisol secretion through an ACTH-independent mechanism. The magnitude of the biological response is influenced by the newly emerged resistance of cortisol receptors, disturbances in intracellular cortisol signaling, and dysregulation between ACTH and cortisol secretion. The detailed study of functional changes in cortisol secretion in response to SARS-CoV-2-associated inflammation provides a new horizon for scientific research following recovery from COVID-19.