Vagus nerve SARS-CoV-2 infection and inflammatory reflex dysfunction: Is there a causal relationship?

Autonomic dysfunction is a clinical hallmark of infection caused by SARS-CoV-2, but the underlying mechanisms are unknown. The vagus nerve inflammatory reflex is an important, well-characterized mechanism for the reflexive suppression of cytokine storm, and its experimental or clinical impairment facilitates the onset and progression of hyperinflammation. Recent pathological evidence from COVID-19 victims reveals viral infection and inflammation in the vagus nerve and associated nuclei in the medulla oblongata. Although it has been suggested that vagus nerve inflammation in these patients mediates dysregulated respiration, whether it also contributes to dysfunction of the vagus nerve inflammatory reflex has not been addressed. Because lethality and tissue injury in acute COVID-19 are characterized by cytokine storm, it is plausible to consider evidence that impairment of the inflammatory reflex may contribute to overproduction of cytokines and resultant hyperinflammatory pathogenesis. Accordingly, here the authors discuss the inflammatory reflex, the consequences of its dysfunction in COVID-19, and whether there are opportunities for therapeutic intervention. image

Automated summary

Autonomic dysfunction is a common feature of SARS-CoV-2 infection, but the mechanisms behind it remain unknown. Recent evidence suggests that viral infection and inflammation in the vagus nerve may contribute to dysregulated respiration and impairment of the vagus nerve inflammatory reflex. This reflex is an important mechanism for suppressing cytokine storm, and its dysfunction may contribute to hyperinflammatory pathogenesis in COVID-19 patients.