Modification of Sympathetic and Hypothalamic Responses to Prevent Complications of COVID-19: “Dam and Wall Concept”

Abstract

We are in the midst of the COVID-19 pandemic. Since December 2019, severe acute respiratory coronavirus (SARS-CoV-2) has infected more than half a billion people, killing nearly 7 million people worldwide. Now various variants of SARS-CoV-2 are causing mayhem and driving the global surge. Epidemiologists are aware of the fact that this virus is capable of escaping immunity and likely to infect the same person multiple times despite adequate vaccination status. Elderly people and those with underlying health conditions who are considered high-risk are likely to suffer complications. While it is tempting to frame complications and mortality from COVID-19 as a simple matter of too much of a virulent virus in too weak of a host, much more is at play here. Framing the pathophysiology of COVID-19 in the context of the Chrousos and Gold model of the stress response system can shed insight into its complex pathogenesis. Understanding the mechanisms of pharmacologic modification of the sympathetic and hypothalamic response system via administration of clonidine and/or dexamethasone may offer an explanation as to why a viral pathogen can be well tolerated and cleared by one host while inflaming and killing another.

Keywords

• stress response system
• sympathetic activity
• HPA (hypothalamic–pituitary–adrenal) axis
• SARS-CoV-2
• catecholamine
• corticosteroids