Display options
Share it on

Semin Immunol. 2021 Jun;55:101545. doi: 10.1016/j.smim.2021.101545. Epub 2021 Nov 27.

Complexity of immune responses in COVID-19.

Seminars in immunology

Michael William Mather, Laura Jardine, Ben Talks, Louis Gardner, Muzlifah Haniffa

Affiliations

  1. Biosciences Institute, Newcastle University, Newcastle upon Tyne, NE2 4HH, UK; Department of Otolaryngology, Freeman Hospital, Newcastle-upon-Tyne Hospitals NHS Foundation Trust, Newcastle-upon-Tyne, NE7 7DN, UK.
  2. Biosciences Institute, Newcastle University, Newcastle upon Tyne, NE2 4HH, UK; Haematology Department, Freeman Hospital, Newcastle-upon-Tyne Hospitals NHS Foundation Trust, Newcastle-upon-Tyne, NE7 7DN, UK.
  3. Biosciences Institute, Newcastle University, Newcastle upon Tyne, NE2 4HH, UK; Department of Dermatology and NIHR Newcastle Biomedical Research Centre, Newcastle Hospitals NHS Foundation Trust, Newcastle upon Tyne, NE2 4LP, UK.
  4. Biosciences Institute, Newcastle University, Newcastle upon Tyne, NE2 4HH, UK; Department of Dermatology and NIHR Newcastle Biomedical Research Centre, Newcastle Hospitals NHS Foundation Trust, Newcastle upon Tyne, NE2 4LP, UK; Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge, CB10 1SA, UK. Electronic address: [email protected].

PMID: 34865933 PMCID: PMC8626289 DOI: 10.1016/j.smim.2021.101545

Abstract

The global COVID-19 pandemic has caused substantial morbidity and mortality to humanity. Remarkable progress has been made in understanding both the innate and adaptive mechanisms involved in the host response to the causative SARS-CoV-2 virus, but much remains to be discovered. Robust upper airway defenses are critical in restricting SARS-CoV-2 replication and propagation. Further, the nasal abundance of viral uptake receptor, ACE2, and the host epithelial transcriptional landscape, are associated with differential disease outcomes across different patient cohorts. The adaptive host response to systemic COVID-19 is heterogeneous and complex. Blunted responses to interferon and robust cytokine generation are hallmarks of the disease, particularly at the advanced stages. Excessive immune cell influx into tissues can lead to substantial collateral damage to the host akin to sepsis. This review offers a contemporary summary of these mechanisms of disease and highlights potential avenues for diagnostic and therapeutic development. These include improved disease stratification, targeting effectors of immune-mediated tissue damage, and blunting of immune cell-mediated tissue damage.

Copyright © 2021. Published by Elsevier Ltd.

Keywords: COVID-19; COVID-19 vaccines; Host microbial interactions; Immune system diseases; Immunity

Substances

MeSH terms

Publication Types

Grant support