GABA administration limits viral replication and pneumonitis in a mouse model of COVID-19

Abstract

Despite the availability of vaccines for COVID-19, serious illness and death induced by coronavirus infection will remain a global health burden because of vaccination hesitancy, possible virus mutations, and the appearance of novel coronaviruses. Accordingly, there is a need for new approaches to limit severe illness stemming from coronavirus infections. Cells of the immune system and lung epithelia express receptors for GABA (GABA-Rs), a widely used neurotransmitter within the CNS. GABA-R agonists have anti-inflammatory effects and can limit acute lung injury. We previously showed that GABA treatment effectively reduced disease severity and death rates in mice following infection with a coronavirus (MHV-1) which provides a potentially lethal model of COVID-19. Here, we report that GABA treatment also reduced viral load in the lungs, suggesting that GABA-Rs may provide a new druggable target to limit pulmonary coronavirus replication. Histopathological analysis revealed that GABA treatment reduced lung inflammatory infiltrates and damages. Since GABA is safe for human consumption, inexpensive, and available worldwide, it is a promising candidate to help treat COVID-19.

Metabolomics-based investigation of SARS-CoV-2 vaccination (Sinovac) reveals an immune-dependent metabolite biomarker

“…Meanwhile, the receptor of GABA (GABA-Rs) plays a pivotal role in the neurotransmission process in the central system. Nevertheless, a recent report revealed that GABA-Rs can be expressed in the immune and epithelial cells as well and showed that GABA treatment can ameliorate inflammation and reduce viral load in the lungs ( 50 ). Simultaneously, our findings identified that GABA and its predecessor metabolite (L-glutamic acid) were significantly upregulated in vaccinated individuals, and GABA also has a significant positive correlation with the serum level of IgG.…”