Human immunopathogenesis of severe acute respiratory syndrome (SARS)
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Progressive immune-associated injury is a hallmark of severe acute respiratory syndrome (SARS). Viral evasion of innate immunity, hypercytokinemia and systemic immunopathology in the SARS coronavirus (SARS CoV) infected host have been suggested as possible mechanisms for the cause of severe pathology and morbidity in SARS patients. The molecular and cellular basis for how SARS CoV impacts the host immune system resulting in severe SARS, however, has not been elucidated. The variable clinical course of SARS may be the result of complex programs of host responses against the infectious agent. Therefore, the systematic analysis of innate and adaptive immune responses to SARS CoV is imperative in building as complete an immunological model as possible of host immunity and inflammatory responses during illness. Here we review recent advances in SARS immunopathogenesis research and present a summary of our findings regarding host responses in SARS patients. We contend that dysregulated type I and II interferon (IFN) responses during SARS may culminate in a failure of the switch from hyper-innate immunity to protective adaptive immune responses in the human host.
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The immune response to coronaviruses induces local and systemic production of cytokines, chemokines and other inflammatory mediators.
“The immune response to coronaviruses induces local and systemic production of cytokines, chemokines, and other inflammatory mediators (Cameron et al., 2008).”
From Anxiety and depression in COVID-19 survivors: role of inflammatory and clinical predictors (2020) · cites this paper as Cameron et al., 2008
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Long COVID and neuropsychiatric manifestations (Review)
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Dysregulated adaptive immune response contributes to severe COVID-19
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Advances in the relationship between coronavirus infection and cardiovascular diseases
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Severe Acute Respiratory Syndrome and Coronavirus
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COVID-19, frailty and long-term care: Implications for policy and practice
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- Authors
- Cameron, M. J., Bermejo-Martin, J. F., Danesh, A., Muller, M. P., & Kelvin, D. J.
- Affiliations
- University Health Network (CA)
- Mount Sinai Hospital (CA)
- Corresponding author
- Kelvin, David J.
- Venue
- Virus Research
- Publisher
- Elsevier BV
- Published
- 2008-04
- Volume
- 133
- Issue
- 1
- Pages
- 13-19
- ISSN
- 0168-1702 (ISSN-L)
- PMC
- PMC7114310
- OpenAlex
- W2076401107
- Cited by
- 391
- References
- 39
- Citations by year
- 2026: 1 · 2025: 6 · 2024: 17 · 2023: 21 · 2022: 65 · 2021: 95 · 2020: 126 · 2019: 3 · 2018: 2 · 2017: 6 · 2016: 5 · 2015: 1 · 2014: 6 · 2013: 2 · 2012: 9
- FWCI
- 4.44
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Virus Research (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Genome Canada
- Ontario Genomics
- Ontario Genomics Institute
- Canadian Institutes of Health Research
- Topics
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Keywords
- SARS, SARS coronavirus, immunopathogenesis, cytokine storm, innate immunity, adaptive immunity, type I interferon, interferon-gamma, viral evasion, host immune response, inflammation
- MeSH terms
- Humans, Immunity, Innate, Models, Biological, Cytokines, Oligonucleotide Array Sequence Analysis, Severe Acute Respiratory Syndrome, Severe acute respiratory syndrome-related coronavirus, Host-Pathogen Interactions
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