Immunological Interfaces: The COVID-19 Pandemic and Depression

Abstract

Since the start of the spread of the coronavirus disease 2019 (COVID-19) pandemic, an international effort has sought to better characterize associated extra-pulmonary health sequelae. The acute and or chronic detrimental impact of SARS-CoV-2 infection on mental health, especially depression, is increasingly described. Simultaneously the pandemic has influenced depressive symptomatology by modifying economic, social and political structures, in addition to affecting daily routines. In both cases, associated immunological perturbations favoring a pro-inflammatory state could underlie an increased risk for depressive symptomatology. A resultant elevation in global depressive burden could further tax mental health care infrastructure and contribute to a range of worse health outcomes including diminished quality of life. This suggests a critical and time-sensitive need to better understand immune interfaces between depression and COVID-19.

Biomarkers of Post-COVID Depression

“…To date, many studies have described an increased level of IL-10 in COVID-19 patients [84][85][86]. In severe cases, the level of IL-10 was higher than in mild cases, and positively correlated with mortality due to COVID-19 [47,85,[87][88][89].…”

“…For COVID-19, the research also diverges. Many studies have shown an increase in the concentration of IFN-γ [84,90,91,105,134,139,140,[144][145][146], however, several studies showed a decrease [47,147,148]. In some studies, the severity of COVID-19 positively correlated with the level of IFN-γ [88,89,131].…”

“…IDO activity is stimulated by pro-inflammatory cytokines such as TNF-α, interferons and prostaglandins. IFN-γ has the strongest stimulating effect on IDO [84]. For this reason, a condition with elevated inflammatory mediators, systemic inflammation, serious infection or trauma predispose to tryptophan transfer to the kynurenine pathway and increased production of its neurotoxic metabolites.…”

Factors Associated with Depression and Anxiety in the Adult Population of Qatar after the First COVID-19 Wave: a Cross-sectional study

“…nancial repercussions) and/or biological consequences of infection is unclear. Neuro-in ammation is one possible biological mechanism by which COVID-19 infection could lead to depression-anxiety (Perlmutter 2021).…”

Effects of β-Blockers on the Sympathetic and Cytokines Storms in Covid-19

“…Notably, involvement of the peripheral nervous system (PNS) and autonomic nervous system (ANS) results in an imbalance between SNS and PSNS with the development of SS ( 23 ). The imbalance of the SNS/PSNS axis of ANS may affect the release of pro-inflammatory cytokines and immune-inflammatory response during Covid-19 ( 24 ). In this context, high circulating catecholamine levels may reflect sympathetic-mediated neutrophilia and T cell dysfunction in Covid-19 due to SS ( 25 ).…”