Interferon β, an enhancer of the innate immune response against SARS-CoV-2 infection

Kali, Suresh Kumar; Dröge, Peter; Murugan, P.

doi:10.1016/j.micpath.2021.105105

Cited by 7 publications

(7 citation statements)

References 93 publications

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“…The signaling begins when it binds with the IFNA receptor and triggers the JAK-STAT pathway, activating interferon-stimulated genes ( ISGs ), such as IFIT1 and IRF1. The upregulation of ISGs simulates an antiviral state, which inhibits viral entry, replication, and translation in both non-infected and infected cells, respectively [ 50 , 51 ].…”

Section: Discussionmentioning

confidence: 99%

Human Genome Polymorphisms and Computational Intelligence Approach Revealed a Complex Genomic Signature for COVID-19 Severity in Brazilian Patients

Pastor

Docena

Rezende

et al. 2023

Viruses

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We present a genome polymorphisms/machine learning approach for severe COVID-19 prognosis. Ninety-six Brazilian severe COVID-19 patients and controls were genotyped for 296 innate immunity loci. Our model used a feature selection algorithm, namely recursive feature elimination coupled with a support vector machine, to find the optimal loci classification subset, followed by a support vector machine with the linear kernel (SVM-LK) to classify patients into the severe COVID-19 group. The best features that were selected by the SVM-RFE method included 12 SNPs in 12 genes: PD-L1, PD-L2, IL10RA, JAK2, STAT1, IFIT1, IFIH1, DC-SIGNR, IFNB1, IRAK4, IRF1, and IL10. During the COVID-19 prognosis step by SVM-LK, the metrics were: 85% accuracy, 80% sensitivity, and 90% specificity. In comparison, univariate analysis under the 12 selected SNPs showed some highlights for individual variant alleles that represented risk (PD-L1 and IFIT1) or protection (JAK2 and IFIH1). Variant genotypes carrying risk effects were represented by PD-L2 and IFIT1 genes. The proposed complex classification method can be used to identify individuals who are at a high risk of developing severe COVID-19 outcomes even in uninfected conditions, which is a disruptive concept in COVID-19 prognosis. Our results suggest that the genetic context is an important factor in the development of severe COVID-19.

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Section: Discussionmentioning

confidence: 99%

Human Genome Polymorphisms and Computational Intelligence Approach Revealed a Complex Genomic Signature for COVID-19 Severity in Brazilian Patients

Pastor

Docena

Rezende

et al. 2023

Viruses

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“…Interferon-β-1a, a cytokine, exhibits an immunogenic response against viral infection ( Yuen et al., 2020 ). Previously, interferon-β-1a showed clinical ineffectiveness against ARDS but exhibited a positive response among the patients of COVID-19 ( Bosi et al., 2020 ; Kali et al., 2021 ; Tortajada et al., 2021 ). Interferon-β-1a, when used during the early stage of infection, reduced the duration of hospitalization and mortality rate ( Davoudi-Monfared et al., 2020 ).…”

Section: Susceptibility Of Coronavirus Disease 2019 To Clinically Used Drugsmentioning

confidence: 99%

Molecular Evolution of Severe Acute Respiratory Syndrome Coronavirus 2: Hazardous and More Hazardous Strains Behind the Coronavirus Disease 2019 Pandemic and Their Targeting by Drugs and Vaccines

Tuli

Sak²,

Aggarwal

et al. 2021

Front. Cell. Infect. Microbiol.

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Within almost the last 2 years, the world has been shaken by the coronavirus disease 2019 (COVID-19) pandemic, which has affected the lives of all people. With nearly 4.92 million deaths by October 19, 2021, and serious health damages in millions of people, COVID-19 has been the most serious global challenge after the Second World War. Besides lost lives and long-term health problems, devastating impact on economics, education, and culture will probably leave a lasting impression on the future. Therefore, the actual extent of losses will become obvious only after years. Moreover, despite the availability of different vaccines and vaccination programs, it is still impossible to forecast what the next steps of the virus are or how near we are to the end of the pandemic. In this article, the route of molecular evolution of the coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is thoroughly compiled, highlighting the changes that the virus has undergone during the last 2 years and discussing the approaches that the medical community has undertaken in the fight against virus-induced damages.

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“…Interferon-β is a naturally-occurring protein produced as an immediate local response to viral infection, and that results in antiviral protein production thereby limiting viral replication [7][8][9]. Importantly, deficiencies in interferon-β-mediated antiviral responses are associated with poorer outcomes in virus challenge studies in patients with COPD [10,11].…”

Section: Introductionmentioning

confidence: 99%

Nebulised interferon beta-1a (SNG001) in the treatment of viral exacerbations of COPD

Monk,

Brookes,

Tear

et al. 2024

Respir Res

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Background Respiratory viral infections are major drivers of chronic obstructive pulmonary disease (COPD) exacerbations. Interferon-β is naturally produced in response to viral infection, limiting replication. This exploratory study aimed to demonstrate proof-of-mechanism, and evaluate the efficacy and safety of inhaled recombinant interferon-β1a (SNG001) in COPD. Part 1 assessed the effects of SNG001 on induced sputum antiviral interferon-stimulated gene expression, sputum differential cell count, and respiratory function. Part 2 compared SNG001 and placebo on clinical efficacy, sputum and serum biomarkers, and viral clearance. Methods In Part 1, patients (N = 13) with stable COPD were randomised 4:1 to SNG001 or placebo once-daily for three days. In Part 2, patients (N = 109) with worsening symptoms and a positive respiratory viral test were randomised 1:1 to SNG001 or placebo once-daily for 14 days in two Groups: A (no moderate exacerbation); B (moderate COPD exacerbation [i.e., acute worsening of respiratory symptoms treated with antibiotics and/or oral corticosteroids]). Results In Part 1, SNG001 upregulated sputum interferon gene expression. In Part 2, there were minimal SNG001–placebo differences in the efficacy endpoints; however, whereas gene expression was initially upregulated by viral infection, then declined on placebo, levels were maintained with SNG001. Furthermore, the proportion of patients with detectable rhinovirus (the most common virus) on Day 7 was lower with SNG001. In Group B, serum C-reactive protein and the proportion of patients with purulent sputum increased with placebo (suggesting bacterial infection), but not with SNG001. The overall adverse event incidence was similar with both treatments. Conclusions Overall, SNG001 was well-tolerated in patients with COPD, and upregulated lung antiviral defences to accelerate viral clearance. These findings warrant further investigation in a larger study. Trial registration EU clinical trials register (2017-003679-75), 6 October 2017.

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Interferon β, an enhancer of the innate immune response against SARS-CoV-2 infection

Cited by 7 publications

References 93 publications

Human Genome Polymorphisms and Computational Intelligence Approach Revealed a Complex Genomic Signature for COVID-19 Severity in Brazilian Patients

Human Genome Polymorphisms and Computational Intelligence Approach Revealed a Complex Genomic Signature for COVID-19 Severity in Brazilian Patients

Molecular Evolution of Severe Acute Respiratory Syndrome Coronavirus 2: Hazardous and More Hazardous Strains Behind the Coronavirus Disease 2019 Pandemic and Their Targeting by Drugs and Vaccines

Nebulised interferon beta-1a (SNG001) in the treatment of viral exacerbations of COPD

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