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Open AccessJournal ArticleDOI

The type I interferon response in COVID-19: implications for treatment.

Jeong Seok Lee, +1 more
- 12 Aug 2020 - 
- Vol. 20, Iss: 10, pp 585-586
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TLDR
Lee et al. as discussed by the authors showed that a robust type I interferon response could exacerbate hyperinflammation in the progression to severe COVID-19 through diverse mechanisms, and further understanding of the roles of type I Interferon at different stages of infection and in patients with mild versus severe CoV-19 will provide insights for the therapeutic use of interferron administration or JAK inhibitors.
Abstract
Despite early reports to the contrary, there is increasing evidence that patients with severe COVID-19 have a robust type I interferon response, which contrasts with the delayed, possibly suppressed, interferon response seen early in infection. A robust type I interferon response could exacerbate hyperinflammation in the progression to severe COVID-19 through diverse mechanisms. Further understanding of the roles of type I interferon at different stages of infection and in patients with mild versus severe COVID-19 will provide insights for the therapeutic use of interferon administration or JAK inhibitors in patients with COVID-19. In this Comment, Jeong Seok Lee and Eui-Cheol Shin discuss contradictory results regarding the downregulation or upregulation of type I interferon responses in patients with COVID-19 and the implications for therapies that target this pathway.

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Citations
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COVID-19 and the human innate immune system.

TL;DR: In this article, a conceptual framework for the interaction of the human innate immune system with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was provided to link the clinical observations with experimental findings that have been made during the first year of the pandemic.
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Immunological mechanisms of vaccine-induced protection against COVID-19 in humans.

TL;DR: Most COVID-19 vaccines have been designed to elicit immune responses, ideally neutralizing antibodies (NAbs), against the SARS-CoV-2 spike protein this article.
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The cGAS–STING pathway drives type I IFN immunopathology in COVID-19

TL;DR: In this article , the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway, which controls immunity to cytosolic DNA, is a critical driver of aberrant type I IFN responses in COVID-19.
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The cGAS–STING pathway drives type I IFN immunopathology in COVID-19

TL;DR: In this paper , the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway, which controls immunity to cytosolic DNA, is a critical driver of aberrant type I IFN responses in COVID-19.
References
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Journal ArticleDOI

Dysregulated Type I Interferon and Inflammatory Monocyte-Macrophage Responses Cause Lethal Pneumonia in SARS-CoV-Infected Mice

TL;DR: Using mice infected with SARS-CoV, it is demonstrated that robust virus replication accompanied by delayed type I interferon (IFN-I) signaling orchestrates inflammatory responses and lung immunopathology with diminished survival and is identified as a potential therapeutic targets in patients infected with pathogenic coronavirus and perhaps other respiratory viruses.
Journal ArticleDOI

A single-cell atlas of the peripheral immune response in patients with severe COVID-19.

TL;DR: Single-cell transcriptomic analysis identifies changes in peripheral immune cells in seven hospitalized patients with COVID-19, including HLA class II downregulation, a heterogeneous interferon-stimulated gene signature and low pro-inflammatory cytokine gene expression in monocytes and lymphocytes.
Related Papers (5)
Trending Questions (1)
Does interferones increased or decreased in covid19 infection?

The paper states that there are contradictory results regarding the type I interferon (IFN-I) response in patients with COVID-19. Some studies report increased expression of IFN-I and interferon-stimulated genes (ISGs), while others report impaired IFN-I responses in severe or critical cases. Therefore, it is unclear whether IFN-I is increased or decreased in COVID-19 infection.