Neuronal and Non-Neuronal GABA in COVID-19: Relevance for Psychiatry

Infection with SARS-CoV-2, the causative agent of COVID-19 pandemic, originated in China and quickly spread across globe. Despite tremendous economic healthcare devastation, research on this virus has contributed to a better understanding numerous molecular pathways, including those involving γ-aminobutyric acid (GABA), that will positively impact medical science, neuropsychiatry, post-pandemic era. SARS-CoV-2 primarily enters host cells through renin–angiotensin system’s component named angiotensin-converting enzyme-2 (ACE-2). Among its many functions, protein upregulates GABA, protecting not only central nervous system but also endothelia, pancreas, gut microbiota. binding ACE-2 usurps neuronal non-neuronal GABAergic systems, contributing high comorbidity neuropsychiatric illness dysbiosis endothelial metabolic dysfunctions. In perspective article, we take closer look at pathology emerging from viral hijacking GABA summarize potential interventions for restoring these systems.