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.
Copyright © 2020 Elsevier Inc. All rights reserved.
MeSH terms
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Angiotensin-Converting Enzyme 2
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Antiviral Agents / therapeutic use*
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Azithromycin / therapeutic use
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Betacoronavirus / drug effects
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Betacoronavirus / immunology
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Betacoronavirus / pathogenicity*
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COVID-19
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Coronavirus Infections / drug therapy*
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Coronavirus Infections / epidemiology
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Coronavirus Infections / immunology
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Coronavirus Infections / virology
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Cytokines / genetics
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Cytokines / immunology
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Disease Management
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Gene Expression Regulation
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Humans
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Hydroxychloroquine / therapeutic use
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Immune Evasion / genetics
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Immune Evasion / immunology
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Immunologic Factors / therapeutic use*
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Pandemics*
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Peptidyl-Dipeptidase A / genetics*
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Peptidyl-Dipeptidase A / immunology
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Pneumonia, Viral / drug therapy*
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Pneumonia, Viral / epidemiology
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Pneumonia, Viral / immunology
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Pneumonia, Viral / virology
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SARS-CoV-2
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Spike Glycoprotein, Coronavirus / genetics*
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Spike Glycoprotein, Coronavirus / immunology
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Toll-Like Receptors / genetics
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Toll-Like Receptors / immunology
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Tumor Necrosis Factor Receptor-Associated Peptides and Proteins / genetics
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Tumor Necrosis Factor Receptor-Associated Peptides and Proteins / immunology
Substances
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Antiviral Agents
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Cytokines
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Immunologic Factors
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Spike Glycoprotein, Coronavirus
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Toll-Like Receptors
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Tumor Necrosis Factor Receptor-Associated Peptides and Proteins
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spike protein, SARS-CoV-2
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Hydroxychloroquine
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Azithromycin
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Peptidyl-Dipeptidase A
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ACE2 protein, human
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Angiotensin-Converting Enzyme 2