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Immune Response, Inflammation, and the Clinical Spectrum of COVID-19
Open accessAbstract
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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“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]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“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]
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“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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Metadata
- Authors
- García, L. F.
- Affiliations
- Universidad de Antioquia (CO)
- Corresponding author
- García, Luis F.
- ORCID
- García, Luis F.
- Venue
- Frontiers in Immunology
- Publisher
- Frontiers Media SA
- Published
- 2020-06-16
- Volume
- 11
- Pages
- 1441-1441
- ISSN
- 1664-3224 (ISSN-L)
- PMC
- PMC7308593
- 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
- gold
- doi.org
- Licence
- 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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