COVID-19 has left mankind desperately seeking how to manage dramatically rising infection rates associated with severe disease progressions. COVID-19 courses range from mild symptoms up to multiple organ failure and death, triggered by excessively high serum cytokine levels (IL 1ß, IL 6, TNF &#945;, IL 8). The vagally driven cholinergic anti-inflammatory pathway (CAP) stops the action of nuclear factor &#954;B (NF-&#954;B), the transcriptional factor of pro-inflammatory cytokines. Thus, well-balanced cytokine release depends on adequate vagal signaling. Coronaviruses replicate using NF-&#954;B transcriptional factor as well. By degrading the cytoplasmatic inhibitor of NF-&#954;B subunits (I&#954;B), coronaviruses induce unrestricted NF-&#954;B expression accelerating both, virus replication and cytokine transcription.We hypothesize that CAP detriment due to depressed vagal tone critically determines the severity of COVID-19.
Autonomic balance determines the severity of COVID-19 courses