Abstract
Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The clinical manifestations of COVID-19 include dry cough, difficult breathing, fever, fatigue, and may lead to pneumonia and respiratory failure. There are significant gaps in the current understanding of whether SARS-CoV-2 attacks the CNS directly or through activation of the peripheral immune system and immune cell infiltration. Although the modality of neurological impairments associated with COVID-19 has not been thoroughly investigated, the latest studies have observed that SARS-CoV-2 induces neuroinflammation and may have severe long-term consequences. Here we review the literature on possible cellular and molecular mechanisms of SARS-CoV-2 induced-neuroinflammation. Activation of the innate immune system is associated with increased cytokine levels, chemokines, and free radicals in the SARS-CoV-2-induced pathogenic response at the blood-brain barrier (BBB). BBB disruption allows immune/inflammatory cell infiltration into the CNS activating immune resident cells (such as microglia and astrocytes). This review highlights the molecular and cellular mechanisms involved in COVID-19-induced neuroinflammation, which may lead to neuronal death. A better understanding of these mechanisms will help gain substantial knowledge about the potential role of SARS-CoV-2 in neurological changes and plan possible therapeutic intervention strategies.
Highlights
The coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
This review summarizes the recent findings that may help understand the link between COVID-19 and neuroinflammation-induced neurological alterations
A study conducted on four COVID-19 patients with coexisting ischemic stroke has shown an elevated D-diameter and Creactive protein level (CRP, a protein produced by the liver in response to inflammation)
Summary
The coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The furin-like cleavage site in SARS-CoV-2 may increase the spreading efficiency of the virus relative to other coronaviruses Both SARS-CoV and SARSCoV-2 use the viral S protein to bind to the ACE2 receptor. The dissociation constant (Kd) between the RBD of SARS-CoV-2 and ACE2 is much lower than that observed with the RBD of SARS-CoV [7, 8] Combined together, these minor differences may play a significant role in the overall activity and severity of the infection of these viruses. MiRNAs can bind to mRNAs, interact with a single or several target genes, and play a critical role in a growing list of pathological conditions, including neurodegenerative diseases, cancer, and cardiovascular disorders. MiR-155 promotes inflammatory processes and negatively regulates BBB function by modulating endothelial cell-to-cell interactions and the interendothelial tight junctions (TJs), such as claudins [37]
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