Coronavirus disease-2019: A review on the disease exacerbation via cytokine storm and concurrent management

https://doi.org/10.1016/j.intimp.2021.108049Get rights and content

Highlights

  • Drug repurposing is the principal treatment strategy against COVID-19 right now.

  • IL-6/1β, CCL2 and complement inhibition are vital in reducing disease exacerbation.

  • NF-κB signaling inhibitors would be the crucial targets in COVID-19 treatment.

Abstract

Setting up treatment strategies is the highest concern today to reduce the fatality of COVID-19. Due to a very new kind of virus attack, no specific treatment has been discovered to date. The most crucial way to dominate the disease severity is now the repurposing of drugs. In this review, we focused on the current treatment approaches targeting the crucial causative factors for the disease burden through cytokine storm or cytokine release syndrome. Several vaccines have been developed and have been applied already for prevention purposes, and several are on the way to be developed, although the effects and side effects are under observation. Presently, regulation of the immune response through intervention treatment methods has been adjusted on the basis of the COVID-19 severity stage and generally includes vaccines, immunotherapies including convalescent plasma and immunoglobulin treatment, monoclonal antibodies, cytokine therapy, complement inhibition, regenerative medicine, and repurposed anti-inflammatory and immune-regulatory drugs. Combination therapy is not acceptable in all respects because there is no concrete evidence in clinical trials or in vivo data. Target-specific drug therapies, such as inhibition of cytokine-producing signaling pathways, could be an excellent solution and thus reduce the severity of inflammation and disease severity. Therefore, gathering information about the mechanism of disease progression, possible goals, and drug efficacy of immune-based approaches to combat COVID-19 in the context of orderly review analysis is consequential.

Keywords

Coronavirus
COVID-19
Cytokine storm
NF-κB
Repurposing of drugs
SARS-CoV-2

Abbreviations

ACE
Angiotensin Converting Enzyme
ADAM-17
Disintegrin and Metallopeptidase Domain
Ag
Angiotensin
APCs
Antigen Presenting Cells
ARDS
Acute Respiratory Distress Syndrome
Cathepsin L
Cathepsin of Lysosome
CLR
C-type lectin receptors
COVID
Coronavirus Disease
CSF
Colony Stimulating Factor
HCoV
Human Corona Virus
HGF
Hepatocyte Growth Factor
IFN
Interferons
IKK
IKb kinase Complex
IL
Interleukins
IP
Inducible Protein
JAK
Janus Kinase
MAPK
Mitogen-activated protein kinase
MAPKK
Mitogen activated Protein Kinase Kinase
MAPKKK/MAP3K
Mitogen activated protein Kinase Kinase Kinase
MAPKs
p38 Mitogen Activated Protein Kinases
MCP
Monocyte Chemoattractant Protein
MERS
Middle East Respiratory Syndrome
MIP
Macrophage Inflammatory Protein
Mpro
main protease
MyD88
Myeloid Differentiation Primary Response dependent
NF-κB
Nuclear Factor kappa B
NK cells
Natural Killer cells
NLR
Nucleotide-binding oligomerization domain-like receptors
nsps
nonstructural proteins
PAMPs
Pathogen Associated Molecular Patterns
PLpro
Papain like protease
PORCN
Porcupine O Acetyl transferase.
pp
polyproteins
PRRs
Pattern Recognition Receptors
RBD
Receptor Binding Domain
RdRp
RNA dependent- RNA polymerase
RIG-1
Retinoic acid inducible gene-1
SARS-CoV-2
Severe Acute Respiratory Syndrome Corona Virus-2 (novel corona virus)
SARS
Severe Acute Respiratory Syndrome
SFRP
Secreted Frizzled related proteins
SP
Spike Protein
STAT
Signal Transducer and Activator of Transcription Proteins
TLR
Toll like Receptor
TMPRSS2
Type II Transmembrane Serine Protease 2
TNF
Tumor Necrosis Factor
TRIF
TLR domain containing adaptor inducing IFN-β
VEGF
Vascular Endothelial Growth Factor
VUI
Variant Under Investigation
WHO
World Health Organization
Wnt
Wingless related Integration site

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