Cited by 740COVID-19 Clinical Research StudiesSARS-CoV-2 and COVID-19 ResearchDermatological and COVID-19 studies

Immune response, inflammation, and the clinical spectrum of COVID-19

Open access
García, Luis F.·2020·Frontiers in Immunology

Abstract

The current COVID-19 pandemic began in December 2019 in Wuhan (China) and rapidly extended to become a global sanitary and economic emergency. Its etiological agent is the coronavirus SARS-CoV-2. COVID-19 presents a wide spectrum of clinical manifestations, which ranges from an asymptomatic infection to a severe pneumonia accompanied by multisystemic failure that can lead to a patient's death. The immune response to SARS-CoV-2 is known to involve all the components of the immune system that together appear responsible for viral elimination and recovery from the infection. Nonetheless, such immune responses are implicated in the disease's progression to a more severe and lethal process. This review describes the general aspects of both COVID-19 and its etiological agent SARS-CoV-2, stressing the similarities with other severe coronavirus infections, such as SARS and MERS, but more importantly, pointing toward the evidence supporting the hypothesis that the clinical spectrum of COVID-19 is a consequence of the corresponding variable spectrum of the immune responses to the virus. The critical point where progression of the disease ensues appears to center on loss of the immune regulation between protective and altered responses due to exacerbation of the inflammatory components. Finally, it appears possible to delineate certain major challenges deserving of exhaustive investigation to further understand COVID-19 immunopathogenesis, thus helping to design more effective diagnostic, therapeutic, and prophylactic strategies.

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Crossref · 10.3389/fimmu.2020.01441

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141 of 146 references verified0 citation errors · 0 not checkable

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  • IL-6 is a major player in chronic inflammatory diseases, autoimmune diseases, cancer and cytokine storm.

    “Among them, IL-6 is a major player in chronic inflammatory diseases, autoimmune diseases, cancer and cytokine storm (1, 3, 10–26).”

    From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [16]

    The Immunological Profile of COVID-19 Patients (page not provided) identifies IL-6 among elevated inflammatory markers in severe COVID-19 and says this inflammatory response may result in cytokine storm. The Changes in Cytokine/Chemokine Plasma Levels section also links higher IL-6 levels to more severe COVID-19. These passages do not establish IL-6 as a major player in chronic inflammatory diseases, autoimmune diseases, or cancer. (LLM, conf=0.87)

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  • Severe COVID-19 is a cytokine storm syndrome.

    “Consistent with the notion that severe COVID-19 is a cytokine storm syndrome (12–17, 336), the severity of COVID-19 is associated with an increased level of inflammatory cytokines, such as IL-6, granulocyte macrophage colony-stimulating factor (GM-CSF) and TNFα (333, 337).”

    From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [16]

    The Clinical-Immunogical Spectrum of COVID-19 section says that immune-response failure can at times lead to cytokine release syndrome with severe inflammation. The Adaptive Immune Response section likewise says a dysfunctional response may lead to a cytokine storm. These passages support the cited notion, but not the unqualified statement that severe COVID-19 is always a cytokine storm syndrome; page numbers were not available in our copy. (LLM, conf=0.82)

    Experimental — accuracy not yet measured
  • ARDS in COVID-19 is considered the result of cytokine storm, resembling the disease caused by SARS-CoV-1 and Middle East respiratory syndrome coronavirus.

    “ARDS in COVID-19 is considered the result of cytokine storm (12–17), resembling the disease caused by SARS-CoV-1 and Middle East respiratory syndrome coronavirus (MERS-CoV) (335).”

    From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [16]

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2 retracted

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Research works printed but not linked: 2

  1. [26]Wertheim JO. A glimpse into the origins of genetic diversity in SARS-CoV-2. Clin Infect Dis. (2020). 10.1093/cid/ciaa213/5780151. [Epub ahead of print]. 32129842 PMC7108145 · DOI
  2. [74]Okba NMA Muller AM Li W Wang C GeurtsvanKessel HC Corman MV. SARS-CoV-2 specific antibody responses in COVID-19 patients. medRxiv. (2020). 10.1101/2020.03.18.2003805932267220 · DOI

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Authors
García, L. F.
Affiliations
Universidad de Antioquia (CO)
Corresponding author
García, Luis F.
Venue
Frontiers in Immunology
Published
2020-06-16
Volume
11
Pages
1441-1441
ISSN
1664-3224 (ISSN-L)
OpenAlex
W3035895802
Cited by
739
References
141
Citations by year
2026: 17 · 2025: 30 · 2024: 68 · 2023: 89 · 2022: 172 · 2021: 279 · 2020: 83
FWCI
7.36
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Immunology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Institutional Repository University of Antioquia (University of Antioquia) (publishedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Greater South Information System
Topics
  • Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
  • Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
  • Health Sciences › Medicine › Dermatology › Dermatological and COVID-19 studies
Keywords
COVID-19 pandemic, SARS-CoV-2, immune response, inflammation, clinical spectrum, immunopathogenesis, disease severity, SARS, MERS, immune regulation, coronavirus infection
MeSH terms
Betacoronavirus, COVID-19, SARS-CoV-2, Age Factors, Antibodies, Viral, Humans, Immunoglobulin A, Secretory, Inflammation, Macrophages, Pneumonia, Viral, T-Lymphocytes, Cytokines, Coronavirus Infections, Antibody-Dependent Enhancement, Pandemics

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