Imbalanced Host Response to SARS-CoV-2 Drives Development of COVID-19
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Abstract
Viral pandemics, such as the one caused by SARS-CoV-2, pose an imminent threat to humanity. Because of its recent emergence, there is a paucity of information regarding viral behavior and host response following SARS-CoV-2 infection. Here we offer an in-depth analysis of the transcriptional response to SARS-CoV-2 compared with other respiratory viruses. Cell and animal models of SARS-CoV-2 infection, in addition to transcriptional and serum profiling of COVID-19 patients, consistently revealed a unique and inappropriate inflammatory response. This response is defined by low levels of type I and III interferons juxtaposed to elevated chemokines and high expression of IL-6. We propose that reduced innate antiviral defenses coupled with exuberant inflammatory cytokine production are the defining and driving features of COVID-19.
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A main evasion strategy seems to be blocking type I interferon responses at several steps, such as viral RNA recognition, nuclear translocation of inflammatory transcription factors, and STAT1/STAT2 phosphorylation.
“A predominant strategy appears to be the inhibition of the type I interferon response58–60 at multiple points, including impaired recognition of viral RNA61,62, decreased nuclear translocation of pro-inflammatory transcription factors (such as IRF3, IRF7 and STAT1)61,63 and suppression of STAT1 and STAT2 phosphorylation64,65.”
From Immunological mechanisms of vaccine-induced protection against COVID-19 in humans (2021) · cites this paper as [59]
SARS-CoV-2 uses a multipronged strategy to antagonize the IFN system, with the clinical consequence of an insufficient type I IFN response in early COVID-19.
“As an immune evasion strategy, SARS-CoV-2 uses a multipronged strategy to antagonize the IFN system with the clinical consequence of an insufficient type I IFN response having been recognized in early COVID-19 studies (Acharya et al., 2020; Blanco-Melo et al., 2020; Sa Ribero et al., 2020).”
From COVID-19 and the human innate immune system (2021) · cites this paper as Blanco-Melo et al., 2020
In in vitro infection models using cell lines, SARS-CoV-2 induced only low type I and II IFNs, consequently inducing moderate levels of ISGs and a unique proinflammatory cytokine signature including IL1B, IL6, TNF, and many chemokines.
“In in vitro infection models utilizing cell lines, SARS-CoV-2 induced only low type I and II IFNs, consequently inducing only moderate levels of ISGs and a unique proinflammatory cytokine signature including IL1B, IL6, and TNF, as well as many chemokines (CCL20, CXCL1, CXCL2, CXCL3, CXCL5, CXCL6, and CXCL16) (Blanco-Melo et al., 2020).”
From COVID-19 and the human innate immune system (2021) · cites this paper as Blanco-Melo et al., 2020
NF-κB-dependent proinflammatory mediators can drive accumulation of pathogenic neutrophils and macrophages in the lung, perpetuating cytokine and chemokine elevation in BALF and circulation.
“Accumulation of NF-κB-dependent proinflammatory mediators can provoke an accumulation of pathogenic inflammatory neutrophils and macrophages in the lung”
From COVID-19 and the human innate immune system (2021) · cites this paper as Blanco-Melo et al., 2020
SARS-CoV-2 is unusually effective at evading or delaying early innate immune responses, including type I and type III IFNs, in vitro and in humans.
“In a SARS-CoV-2 infection, the virus is particularly effective at avoiding or delaying triggering intracellular innate immune responses associated with type I and type III IFNs in vitro (Blanco-Melo et al., 2020) and in humans (Arunachalam et al., 2020; Bastard et al., 2020; Blanco-Melo et al., 2020; Laing et al., 2020).”
From Adaptive immunity to SARS-CoV-2 and COVID-19 (2021) · cites this paper as Blanco-Melo et al., 2020
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- Authors
- Blanco-Melo, D., Nilsson-Payant, B. E., Liu, W.-C., Uhl, S., Hoagland, D., Møller, R., Jordan, T. X., Oishi, K., Panis, M., Sachs, D., Wang, T. T., Schwartz, R. E., Lim, J. K., Albrecht, R. A., & tenOever, B. R.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- Chan Zuckerberg Biohub San Francisco (US)
- Weill Cornell Medicine (US)
- Corresponding author
- Schwartz, Robert E.
- Lim, Jean K.
- Albrecht, Randy A.
- tenOever, Benjamin R.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2020-05
- Volume
- 181
- Issue
- 5
- Pages
- 1036-1045.e9
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC7227586
- OpenAlex
- W3016489853
- Cited by
- 4,222
- References
- 51
- Citations by year
- 2026: 149 · 2025: 217 · 2024: 357 · 2023: 497 · 2022: 847 · 2021: 1338 · 2020: 810 · 2019: 2 · 2017: 1 · 2013: 1 · 2012: 1
- FWCI
- 115.47
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (am, 392 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (acceptedVersion)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by-nd)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Public Health Service
- National Institutes of Health
- Defense Advanced Research Projects Agency
- National Institute of Allergy and Infectious Diseases
- Topics
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Keywords
- SARS-CoV-2, COVID-19 pandemic, host response, transcriptional response, type I interferon, interferon lambda, chemokines, interleukin-6, inflammatory cytokines, antiviral innate immunity, respiratory viruses, viral infection
- MeSH terms
- Betacoronavirus, COVID-19, SARS-CoV-2, Animals, Cells, Cultured, Disease Models, Animal, Humans, Immunity, Innate, Inflammation, Interferons, Pneumonia, Viral, RNA Viruses, Transcription, Genetic, Coronavirus Infections, Chemokines, Host-Pathogen Interactions, Pandemics
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