New data may provide answers for those experiencing persistent symptoms long after their bout with COVID-19 has ended. These may include fatigue, lightheadedness, brain fog, cognitive issues, gastrointestinal problems, heart palpitations, shortness of breath, or an inability to tolerate upright postures.
A July 15 study published in Acta Neuropathologica suggests that SARS-CoV-2 infection may damage the nerves of the autonomic nervous system (ANS), causing an inflammatory response that can later lead to dysautonomia observed in long COVID patients.
Using several methods, researchers at the University Medical Center Hamburg-Eppendorf in Germany performed a microscopic analysis of the vagus nerves in 27 deceased patients with COVID-19 and five controls who died of other causes, without COVID-19.
The vagus nerve is a vital component of the ANS that regulates critical functions such as digestion, respiratory and heart rate, and immune response. Vagus nerve signaling to the brainstem also controls the “sickness behavior response,” where the brain mounts flu-like symptoms including nausea, fatigue, pain, and other chronic symptoms in response to inflammation.
The researchers detected SARS-CoV-2 RNA in vagus nerve samples obtained from deceased patients with severe COVID-19 showing direct infection of the nerve was accompanied by inflammatory cell infiltration composed mostly of monocytes—a type of white blood cell that finds and destroys germs and eliminates infected cells. Their analysis revealed a “strong enrichment of genes regulating antiviral responses and interferon signaling,” supporting the idea that vagus nerve inflammation is a common phenomenon with COVID-19.