Review Article
COVID-19: Immunology and treatment options

https://doi.org/10.1016/j.clim.2020.108448Get rights and content

Highlights

  • SARS-CoV2 can escape the immune system by suppressing innate anti-viral responses

  • Tissue damage and antibody dependent enhancement can promote a cytokine storm

  • Unfavorable outcomes associate with features of cytokine storm syndrome

  • Host factors, including age, affect the individual’s prognosis

  • Immune modulating treatment should be considered and tested prospectively

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.

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