ArticleCytokine2021
ACE2 expression is related to the interferon response in airway epithelial cells but is that functional for SARS-CoV-2 entry?
Article in Cytokine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Review
- Zebrafish models of COVID-19.FEMS microbiology reviews · 2023Review
- Article
- Regulation of IFNα-induced expression of the short ACE2 isoform by ULK1.Molecular immunology · 2022Article
- Anti-IFN-α/-ω neutralizing antibodies from COVID-19 patients correlate with downregulation of IFN response and laboratory biomarkers of disease severity.European journal of immunology · 2022Article
- Liver damage in the context of SARS-CoV-2. Covid-19 treatment and its effects on the liver.Journal of medicine and life · 2022Review
- Distribution ofMicroorganisms · 2022Article
- The impact of coronavirus SARS-CoV-2 (COVID-19) in water: potential risks.Environmental science and pollution research international · 2021Review
- Innate Immunity in Children and the Role of ACE2 Expression in SARS-CoV-2 Infection.Pediatric reports · 2021Review
- The Impact of Angiotensin-Converting Enzyme 2 (ACE2) Expression on the Incidence and Severity of COVID-19 Infection.Pathogens (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In vitro interferon (IFN)α treatment of primary human upper airway basal cells has been shown to drive ACE2 expression, the receptor of SARS-CoV-2. The protease furin is also involved in mediating SARS-CoV-2 and other viral infections, although its association with early IFN response has not been evaluated yet. In order to assess the in vivo relationship between ACE2 and furin expression and the IFN response in nasopharyngeal cells, we first examined ACE2 and furin levels and their correlation with the well-known marker of IFNs' activation, ISG15, in children (n = 59) and adults (n = 48), during respiratory diseases not caused by SARS-CoV-2. A strong positive correlation was found between ACE2 expression, but not of furin, and ISG15 in all patients analyzed. In addition, type I and III IFN stimulation experiments were performed to examine the IFN-mediated activation of ACE2 isoforms (full-length and truncated) and furin in epithelial cell lines. Following all the IFNs treatments, only the truncated ACE2 levels, were upregulated significantly in the A549 and Calu3 cells, in particular by type I IFNs. If confirmed in vivo following IFNs' activation, the induction of the truncated ACE2 isoform only would not enhance the risk of SARS-CoV-2 infection in the respiratory tract.
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