Immune responses during COVID-19 infection

Oncoimmunology. 2020 Aug 25;9(1):1807836. doi: 10.1080/2162402X.2020.1807836.

Abstract

Over the past 16 years, three coronaviruses (CoVs), severe acute respiratory syndrome CoV (SARS-CoV) in 2002, Middle East respiratory syndrome CoV (MERS-CoV) in 2012 and 2015, and SARS-CoV-2 in 2020, have been causing severe and fatal human epidemics. The unpredictability of coronavirus disease-19 (COVID-19) poses a major burden on health care and economic systems across the world. This is caused by the paucity of in-depth knowledge of the risk factors for severe COVID-19, insufficient diagnostic tools for the detection of SARS-CoV-2, as well as the absence of specific and effective drug treatments. While protective humoral and cellular immune responses are usually mounted against these betacoronaviruses, immune responses to SARS-CoV2 sometimes derail towards inflammatory tissue damage, leading to rapid admissions to intensive care units. The lack of knowledge on mechanisms that tilt the balance between these two opposite outcomes poses major threats to many ongoing clinical trials dealing with immunostimulatory or immunoregulatory therapeutics. This review will discuss innate and cognate immune responses underlying protective or deleterious immune reactions against these pathogenic coronaviruses.

Keywords: Coronavirus; Covid-19; Sars-CoV-2; cellular; humoral; immune response; immunity.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • COVID-19 / diagnosis
  • COVID-19 / immunology*
  • COVID-19 / virology
  • Host Microbial Interactions / immunology*
  • Humans
  • Immunity, Cellular
  • Immunity, Humoral
  • Middle East Respiratory Syndrome Coronavirus / immunology
  • Protective Factors
  • Risk Factors
  • SARS-CoV-2 / immunology*
  • Severe acute respiratory syndrome-related coronavirus / immunology
  • Severity of Illness Index

Grants and funding

ONCOVID was supported by Dassault Systems, Izipizi, Agnès b., Ralph Lauren and Malakoff Humanis, Sanofi. LZ and GK were supported by the Ligue contre le Cancer (équipe labelisée); Agence National de la Recherche (ANR) – Projets blancs; ANR under the frame of E-Rare-2, the ERA-Net for Research on Rare Diseases; Association pour la recherche sur le cancer (ARC); Cancéropôle Ile-de-France; Chancelerie des universités de Paris (Legs Poix), Fondation pour la Recherche Médicale (FRM); a donation by Elior; the European Commission (Horizon 2020: Oncobiome); the European Research Council (ERC); Institut National du Cancer (INCa); Inserm (HTE); Institut Universitaire de France; LeDucq Foundation; the LabEx Immuno-Oncology; the RHU Torino Lumière; the Seerave Foundation; the SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination (SOCRATE); ONCOBIOME H2020 network, and the SIRIC Cancer Research and Personalized Medicine (CARPEM); RHU Torino Lumière (ANR-16-RHUS-0008) and CARE (directed by X. Mariette). Cléa Melenotte was supported by the RHU Lumière for its post doctoral fellowship.