SARS-CoV-2 Causes a Different Cytokine Response Compared to Other Cytokine Storm-Causing Respiratory Viruses in Severely Ill Patients.
COVID-19
/ blood
Cytokine Release Syndrome
/ blood
Cytokines
/ blood
Humans
Inflammation
/ immunology
Influenza A virus
/ immunology
Influenza, Human
/ blood
Middle East Respiratory Syndrome Coronavirus
/ immunology
Severe acute respiratory syndrome-related coronavirus
/ immunology
SARS-CoV-2
/ immunology
Severe Acute Respiratory Syndrome
/ blood
Severity of Illness Index
MERS- and SARS-CoV
SARS-CoV-2
cytokine response
influenza A
literature analysis
systematic review
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2021
2021
Historique:
received:
20
11
2020
accepted:
29
01
2021
entrez:
18
3
2021
pubmed:
19
3
2021
medline:
2
4
2021
Statut:
epublish
Résumé
Hyper-induction of pro-inflammatory cytokines, also known as a cytokine storm or cytokine release syndrome (CRS), is one of the key aspects of the currently ongoing SARS-CoV-2 pandemic. This process occurs when a large number of innate and adaptive immune cells activate and start producing pro-inflammatory cytokines, establishing an exacerbated feedback loop of inflammation. It is one of the factors contributing to the mortality observed with coronavirus 2019 (COVID-19) for a subgroup of patients. CRS is not unique to the SARS-CoV-2 infection; it was prevalent in most of the major human coronavirus and influenza A subtype outbreaks of the past two decades (H5N1, SARS-CoV, MERS-CoV, and H7N9). With a comprehensive literature search, we collected changing the cytokine levels from patients upon infection with the viral pathogens mentioned above. We analyzed published patient data to highlight the conserved and unique cytokine responses caused by these viruses. Our curation indicates that the cytokine response induced by SARS-CoV-2 is different compared to other CRS-causing respiratory viruses, as SARS-CoV-2 does not always induce specific cytokines like other coronaviruses or influenza do, such as IL-2, IL-10, IL-4, or IL-5. Comparing the collated cytokine responses caused by the analyzed viruses highlights a SARS-CoV-2-specific dysregulation of the type-I interferon (IFN) response and its downstream cytokine signatures. The map of responses gathered in this study could help specialists identify interventions that alleviate CRS in different diseases and evaluate whether they could be used in the COVID-19 cases.
Identifiants
pubmed: 33732251
doi: 10.3389/fimmu.2021.629193
pmc: PMC7956943
doi:
Substances chimiques
Cytokines
0
Types de publication
Research Support, Non-U.S. Gov't
Systematic Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
629193Subventions
Organisme : Biotechnology and Biological Sciences Research Council
ID : BBS/E/F/000PR10355
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/N023781/1
Pays : United Kingdom
Informations de copyright
Copyright © 2021 Olbei, Hautefort, Modos, Treveil, Poletti, Gul, Shannon-Lowe and Korcsmaros.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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