Triangle of cytokine storm, central nervous system involvement, and viral infection in COVID-19: the role of sFasL and neuropilin-1
Author:
Saleki Kiarash123ORCID, Banazadeh Mohammad4, Miri Niloufar Sadat5, Azadmehr Abbas356
Affiliation:
1. Student Research Committee, Babol University of Medical Sciences , Babol , 47176-47745 , Iran 2. USERN Office, Babol University of Medical Sciences , Babol , 47176-47745 , Iran 3. National Elite Foundation, Mazandaran Province Branch , Tehran , 48157-66435 , Iran 4. Pharmaceutical Sciences and Cosmetic Products Research Center , Kerman University of Medical Sciences , Kerman , 76169-13555 , Iran 5. Cellular and Molecular Biology Research Center , Health Research Institute, Babol University of Medical Sciences , Babol , 47176-47745 , Iran 6. Medical Immunology Department , Babol University of Medical Sciences , Babol , 47176-47745 , Iran
Abstract
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) is identified as the cause of coronavirus disease 2019 (COVID-19), and is often linked to extreme inflammatory responses by over activation of neutrophil extracellular traps (NETs), cytokine storm, and sepsis. These are robust causes for multi-organ damage. In particular, potential routes of SARS-CoV2 entry, such as angiotensin-converting enzyme 2 (ACE2), have been linked to central nervous system (CNS) involvement. CNS has been recognized as one of the most susceptible compartments to cytokine storm, which can be affected by neuropilin-1 (NRP-1). ACE2 is widely-recognized as a SARS-CoV2 entry pathway; However, NRP-1 has been recently introduced as a novel path of viral entry. Apoptosis of cells invaded by this virus involves Fas receptor–Fas ligand (FasL) signaling; moreover, Fas receptor may function as a controller of inflammation. Furthermore, NRP-1 may influence FasL and modulate cytokine profile. The neuroimmunological insult by SARS-CoV2 infection may be inhibited by therapeutic approaches targeting soluble Fas ligand (sFasL), cytokine storm elements, or related viral entry pathways. In the current review, we explain pivotal players behind the activation of cytokine storm that are associated with vast CNS injury. We also hypothesize that sFasL may affect neuroinflammatory processes and trigger the cytokine storm in COVID-19.
Publisher
Walter de Gruyter GmbH
Subject
General Neuroscience
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