Elsevier

Clinical Immunology

Volume 222, January 2021, 108615
Clinical Immunology

Review Article
An enlightening role for cytokine storm in coronavirus infection

https://doi.org/10.1016/j.clim.2020.108615Get rights and content

Highlights

  • In December 2019, a novel coronavirus of SARS-CoV-2hit Wuhan, Hubei, China, and then spread globally.

  • SARS-CoV-2 generally causes a mild lower respiratory infection in humans, however, in some severe cases, multiple organ dysfunction occurs.

  • Overproduction of cytokines, termed cytokine storm, may involve in disease progression and even be responsible for deaths.

  • Application of immune-modulators might become a complement to support treatment and flip on the light switch for severe patients.

Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) outbreak in Wuhan, China has dispersed rapidly worldwide. Although most patients present with mild fever, cough with varying pulmonary shadows, a significant portion still develops severe respiratory dysfunction. And these severe cases are often associated with manifestations outside the respiratory tract. Currently, it is not difficult to find inflammatory cytokines upregulated in the blood of infected patients. However, some complications in addition to respiratory system with the coronavirus disease 2019 (COVID-19) are impossible to explain or cannot be attributed to virus itself. Thus excessive cytokines and their potentially fatal adverse effects are probably the answer to the multiple organ dysfunctions and growing mortality. This review provides a comprehensive overview of the mechanisms underlying cytokine storm, summarizes its pathophysiology and improves understanding of cytokine storm associated with coronavirus infections by comparing SARS-CoV-2 with severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV).

Keywords

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
Inflammatory cytokines
Coronavirus disease 2019 (COVID-19)
Multiple organ dysfunctions
Cytokine storm

Abbreviations

SARS-CoV-2
severe acute respiratory syndrome coronavirus 2
CoV
coronavirus
WHO
World Health Organization
ALI
acute lung injury
ARDS
acute respiratory distress syndrome
CNS
central nervous system
COVID-19
coronavirus disease 2019
MERS
Middle East respiratory syndrome
SARS
severe acute respiratory syndrome
IL
interleukin
IFN
interferons
TNF
tumor necrosis factor
MCP
monocyte chemoattractant protein
IL-1RA
IL-1 receptor antagonist
IP-10
IFN-γ-inducible protein-10
Th
helper T cell
DC
dendritic cell
NK
natural killer cell
B
B lymphocyte
Th2
T-helper-2 cell
BMSC
bone marrow stromal cell
Th1
T-helper-1 cell
PBMC
peripheral blood mononuclear cell
CCL
chemokine ligand
CXCL
chemokine (C-X-C motif) ligand
GCSF
granulocyte colony stimulating factor
GMCSF
granulocyte-macrophage colony-stimulating factor
FGF
fibroblast growth factor
PDGF
platelet derived growth factor
VEGF
vascular endothelial cell growth factor
MIP1A
macrophage Inflammatory Protein 1 Alpha
MIP1B
macrophage Inflammatory Protein 1 beta
PRRs
pattern recognition receptors
TLRs
Toll-like receptors
PAMPs
pathogen-associated molecular patterns
CRP
C-reactive protein
NLR
neutrophil-to-lymphocyte ratio
COVID-CSS
COVID-19 related cytokine storm syndrome
ACE2
angiotensin-converting enzyme 2
NF-κB
nuclear factor κB
JAK
Janus kinase
STAT
signal transducer and activator of transcription
IRF3
IFN regulatory factor-3

Cited by (0)

1

First author: Zhongyi Zhao, Email: [email protected]

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