SARS-CoV-2 consequences for mental health: Neuroinflammatory pathways linking COVID-19 to anxiety and depression

The coronavirus disease 2019 (COVID-19) pandemic has been linked to an increased prevalence of mental health disorders, particularly anxiety and depression. Moreover, the COVID-19 pandemic has caused stress in people worldwide due to several factors, including fear of infection; social isolation; difficulty in adapting to new routines; lack of coping methods; high exposure to social media, misinformation, and fake reports; economic impact of the measures implemented to slow the contagion and concerns regarding the disease pathogenesis. COVID-19 patients have elevated levels of pro-inflammatory cytokines, such as interleukin (IL)-1 beta, IL-6, and tumor necrosis factor-alpha, and other inflammation-related factors. Furthermore, invasion of the central nervous system by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may potentially contribute to neuroinflammatory alterations in infected individuals. Neuroinflammation, a consequence of psychological stress due to the COVID-19 pandemic, may also play a role in the development of anxiety and depressive symptoms in the general population. Considering that neuroinflammation plays a significant role in the pathophysiology of depression and anxiety, this study investigated the effects of SARS-CoV-2 on mental health and focused on the impact of the COVID-19 pandemic on the neuroinflammatory pathways. (C) The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.

Automated summary

The COVID-19 pandemic is associated with an increased prevalence of mental health disorders, particularly anxiety and depression. The pandemic has caused stress due to factors such as fear of infection, social isolation, difficulty in adapting to new routines, misinformation, and economic impact. COVID-19 patients have elevated levels of pro-inflammatory cytokines, and the virus may invade the central nervous system, potentially leading to neuroinflammatory alterations.