COVID-19 in patients with systemic lupus erythematosus: lessons learned from the inflammatory disease

Transl Res. 2021 Jun:232:13-36. doi: 10.1016/j.trsl.2020.12.007. Epub 2020 Dec 19.

Abstract

As the world navigates the coronavirus disease 2019 (COVID-19) pandemic, there is a growing need to assess its impact in patients with autoimmune rheumatic diseases, such as systemic lupus erythematosus (SLE). Patients with SLE are a unique population when considering the risk of contracting COVID-19 and infection outcomes. The use of systemic glucocorticoids and immunosuppressants, and underlying organ damage from SLE are potential susceptibility factors. Most patients with SLE have evidence of high type I interferon activity, which may theoretically act as an antiviral line of defense or contribute to the development of a deleterious hyperinflammatory response in COVID-19. Other immunopathogenic mechanisms of SLE may overlap with those described in COVID-19, thus, studies in SLE could provide some insight into immune responses occurring in severe cases of the viral infection. We reviewed the literature to date on COVID-19 in patients with SLE and provide an in-depth review of current research in the area, including immune pathway activation, epidemiology, clinical features, outcomes, and the psychosocial impact of the pandemic in those with autoimmune disease.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Antibodies, Antiphospholipid / immunology
  • COVID-19 / epidemiology
  • COVID-19 / etiology*
  • COVID-19 / immunology
  • Complement System Proteins / physiology
  • Extracellular Traps / physiology
  • Health Services Accessibility
  • Humans
  • Interferon Type I / physiology
  • Lupus Erythematosus, Systemic / complications*
  • Lupus Erythematosus, Systemic / immunology
  • SARS-CoV-2*
  • TOR Serine-Threonine Kinases / physiology

Substances

  • Antibodies, Antiphospholipid
  • Interferon Type I
  • Complement System Proteins
  • TOR Serine-Threonine Kinases