COVID-19: Immunology and treatment options

Susanna Felsenstein; Jenny A Herbert; Paul S McNamara; Christian M Hedrich

doi:10.1016/j.clim.2020.108448

COVID-19: Immunology and treatment options

Clin Immunol. 2020 Jun:215:108448. doi: 10.1016/j.clim.2020.108448. Epub 2020 Apr 27.

Authors

Susanna Felsenstein¹, Jenny A Herbert², Paul S McNamara², Christian M Hedrich³

Affiliations

¹ Department of Infectious Diseases and Immunology, Alder Hey Children's NHS Foundation Trust Hospital, Liverpool, UK.
² Department of Women's & Children's Health, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
³ Department of Women's & Children's Health, Institute of Translational Medicine, University of Liverpool, Liverpool, UK; Department of Paediatric Rheumatology, Alder Hey Children's NHS Foundation Trust Hospital, Liverpool, UK. Electronic address: christian.hedrich@liverpool.ac.uk.

Abstract

The novel coronavirus SARS-CoV2 causes COVID-19, a pandemic threatening millions. As protective immunity does not exist in humans and the virus is capable of escaping innate immune responses, it can proliferate, unhindered, in primarily infected tissues. Subsequent cell death results in the release of virus particles and intracellular components to the extracellular space, which result in immune cell recruitment, the generation of immune complexes and associated damage. Infection of monocytes/macrophages and/or recruitment of uninfected immune cells can result in massive inflammatory responses later in the disease. Uncontrolled production of pro-inflammatory mediators contributes to ARDS and cytokine storm syndrome. Antiviral agents and immune modulating treatments are currently being trialled. Understanding immune evasion strategies of SARS-CoV2 and the resulting delayed massive immune response will result in the identification of biomarkers that predict outcomes as well as phenotype and disease stage specific treatments that will likely include both antiviral and immune modulating agents.

Publication types

Review

MeSH terms

Angiotensin-Converting Enzyme 2
Antiviral Agents / therapeutic use*
Azithromycin / therapeutic use
Betacoronavirus / drug effects
Betacoronavirus / immunology
Betacoronavirus / pathogenicity*
COVID-19
Coronavirus Infections / drug therapy*
Coronavirus Infections / epidemiology
Coronavirus Infections / immunology
Coronavirus Infections / virology
Cytokines / genetics
Cytokines / immunology
Disease Management
Gene Expression Regulation
Humans
Hydroxychloroquine / therapeutic use
Immune Evasion / genetics
Immune Evasion / immunology
Immunologic Factors / therapeutic use*
Pandemics*
Peptidyl-Dipeptidase A / genetics*
Peptidyl-Dipeptidase A / immunology
Pneumonia, Viral / drug therapy*
Pneumonia, Viral / epidemiology
Pneumonia, Viral / immunology
Pneumonia, Viral / virology
SARS-CoV-2
Spike Glycoprotein, Coronavirus / genetics*
Spike Glycoprotein, Coronavirus / immunology
Toll-Like Receptors / genetics
Toll-Like Receptors / immunology
Tumor Necrosis Factor Receptor-Associated Peptides and Proteins / genetics
Tumor Necrosis Factor Receptor-Associated Peptides and Proteins / immunology

Substances

Antiviral Agents
Cytokines
Immunologic Factors
Spike Glycoprotein, Coronavirus
Toll-Like Receptors
Tumor Necrosis Factor Receptor-Associated Peptides and Proteins
spike protein, SARS-CoV-2
Hydroxychloroquine
Azithromycin
Peptidyl-Dipeptidase A
ACE2 protein, human
Angiotensin-Converting Enzyme 2