Exploring New Mechanism of Depression from the Effects of Virus on Nerve Cells

Abstract

Depression is a common neuropsychiatric disorder with long-term recurrent depressed mood, pain and despair, pessimism and anxiety, and even suicidal tendencies as the main symptoms. Depression usually induces or aggravates the development of other related diseases, such as sleep disorders and endocrine disorders. In today’s society, the incidence of depression is increasing worldwide, and its pathogenesis is complex and generally believed to be related to genetic, psychological, environmental, and biological factors. Current studies have shown the key role of glial cells in the development of depression, and it is noteworthy that some recent evidence suggests that the development of depression may be closely related to viral infections, such as SARS-CoV-2, BoDV-1, ZIKV, HIV, and HHV6, which infect the organism and cause some degree of glial cells, such as astrocytes, oligodendrocytes, and microglia. This can affect the transmission of related proteins, neurotransmitters, and cytokines, which in turn leads to neuroinflammation and depression. Based on the close relationship between viruses and depression, this paper provides an in-depth analysis of the new mechanism of virus-induced depression, which is expected to provide a new perspective on the mechanism of depression and a new idea for the diagnosis of depression in the future.

The Thr92Ala polymorphism in the type 2 deiodinase gene is linked to depression in patients with COVID-19 after hospital discharge

“…Microglial cells, specific types of macrophages in the central nervous system, play a crucial role in neuroinflammation and are increasingly linked to the development of depression. Recent findings suggest a potential link between depression onset and viral infections like SARS-CoV-2, BoDV-1, ZIKV, HIV, and HHV6, which impact various glial cells, including astrocytes, oligodendrocytes, and microglia ( 48 ). Transcriptomic analysis [Gene Set Enrichment Analysis (GSEA)] of mice with the Thr92Ala polymorphism revealed increased gene expression related to neuroplasticity, cognition, apoptosis, and neuroinflammation.…”

Exploring the Pathophysiology of Long COVID: The Central Role of Low-Grade Inflammation and Multisystem Involvement

“…Currently, functional changes in the CNS are prominent in LC symptomatology. The role of microglial activation linked to viral infections in the development of mild neuroinflammation (neuroparainflammation) is undeniable, not only in the pathogenesis of neurodegenerative diseases and accelerated brain aging [ 201 , 202 , 203 ] but also in canonical neuropsychiatric diseases such as schizophrenia and depression [ 204 , 205 , 206 ]. Moreover, the molecular mechanisms of cellular and tissue proinflammatory stress manifest not only in pathologies but also support many physiological processes of the CNS.…”

“…Importantly, ME/CFS can be caused by localized low-grade inflammation in specific parts of the central nervous system, including latent chronic viral infections and post-viral conditions. Enteroviruses and herpesviruses, such as EBV, HHV-6, and CMV, are considered potential etiological factors for viral ME/CFS [ 46 , 205 , 206 ]. Extensive evidence now links ME/CFS to LC [ 222 , 223 , 224 , 225 , 226 , 227 , 228 ].…”