Microbiota-Gut-Brain Communication in the SARS-CoV-2 Infection

Abstract

The coronavirus disease of 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome 2 (SARS-CoV-2). In addition to pneumonia, individuals affected by the disease have neurological symptoms. Indeed, SARS-CoV-2 has a neuroinvasive capacity. It is known that the infection caused by SARS-CoV-2 leads to a cytokine storm. An exacerbated inflammatory state can lead to the blood–brain barrier (BBB) damage as well as to intestinal dysbiosis. These changes, in turn, are associated with microglial activation and reactivity of astrocytes that can promote the degeneration of neurons and be associated with the development of psychiatric disorders and neurodegenerative diseases. Studies also have been shown that SARS-CoV-2 alters the composition and functional activity of the gut microbiota. The microbiota-gut-brain axis provides a bidirectional homeostatic communication pathway. Thus, this review focuses on studies that show the relationship between inflammation and the gut microbiota–brain axis in SARS-CoV-2 infection.

Repeated ethanol exposure and withdrawal alters ACE2 expression in discrete brain regions: Implications for SARS-CoV-2 infection

“…Interestingly, we observed an increase in the ACE2 and a non-significant change in TMPRSS2 after CIE, suggesting a high risk for SARS-CoV-2 infection in individuals with AUD. Another possible route for viral neuroinvasion could be from the gut through the vagus nerve (Guo et al, 2021; Manosso et al, 2021) and clinical reports show prominent staining for SARS-CoV-2 in the vagus nerve fibers (Bulfamante et al, 2021). Within the CNS, the vagus nerve primarily projects to NTS, releasing excitatory/inhibitory neurotransmitters, acetylcholine, norepinephrine, and neuropeptides.…”

Can SARS-CoV-2 Infection Exacerbate Alzheimer’s Disease? An Overview of Shared Risk Factors and Pathogenetic Mechanisms

“…The authors observed higher levels of gut permeability markers and the presence of microbes in the plasma of patients compared to controls. It is well known that the translocation of fecal microbiota into systemic circulation could be a key driver of immune response and inflammation [114][115][116][117], and thus may contribute to worsening COVID-19 outcomes [118].…”

Infection of Human Cells by SARS-CoV-2 and Molecular Overview of Gastrointestinal, Neurological, and Hepatic Problems in COVID-19 Patients

“…Dietary tryptophan is primarily absorbed via the transport pathway of B0AT1/ACE2 in the epithelial cells of the small intestinal; this results in mTOR pathway activation and the regulation of the expression of antimicrobial peptides. These peptides can adjust the gut microbiota composition [ 67 ]. The blocking of ACE2 and aberrant mTOR activity after SARS-COV-2 infection can molecularly explain how amino acid malnutrition results in intestinal inflammation and diarrhea.…”

“…The blocking of ACE2 and aberrant mTOR activity after SARS-COV-2 infection can molecularly explain how amino acid malnutrition results in intestinal inflammation and diarrhea. As SARS-CoV-2 S protein binds to the ACE2 receptor, blocking ACE2 leads to B0AT1 being blocked and thus tryptophan absorption being disturbed, leading to the alteration of the microbiota due to the aberrant secretion of antimicrobial peptides [ 67 ]. Hence, aberrant mTOR activity leads to a decreased expression of antimicrobial peptides from small intestinal Paneth cells ( Figure 3 ).…”