ArticleViruses2015
Glucose-6-Phosphate Dehydrogenase Enhances Antiviral Response through Downregulation of NADPH Sensor HSCARG and Upregulation of NF-κB Signaling.
Article in Viruses, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 35 citations in OpenAlex.
- Host Cell Central Carbon Metabolism and Cellular NADViruses · 2026Article
- NMRAL1 as a Causal Factor in Postherpetic Neuralgia: A Proteome-Wide Mendelian Randomization Study.Journal of pain research · 2025Article
- [The effect of glucose-6-phosphate dehydrogenase deficiency on allogeneic hematopoietic stem cell transplantation in patients with hematological disorders].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2024Article
- Glucose-6-Phosphate Dehydrogenase Deficiency and Coronavirus Disease 2019.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2023Article
- G6PD deficiency-does it alter the course of COVID-19 infections?Annals of hematology · 2023Review
- Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency and Long-Term Risk of Immune-Related diseases.medRxiv : the preprint server for health sciences · 2023Article
- Association of Glucose-6-Phosphate Dehydrogenase Deficiency With Outcomes in US Veterans With COVID-19.JAMA network open · 2023Article
- Glucose-6-phosphate dehydrogenase deficiency and long-term risk of immune-related disorders.Frontiers in immunology · 2023Observational
- Article
- Hematologic Outcomes of COVID-19 Patients with and without G6PD Deficiency: A Comparative Study.Qatar medical journal · 2022Article
- Association between Glucose-6-Phosphate Dehydrogenase Deficiency and Asthma.Journal of clinical medicine · 2021Article
- Current investigations on clinical pharmacology and therapeutics of Glucose-6-phosphate dehydrogenase deficiency.Pharmacology & therapeutics · 2021Review
- G6PD deficiency, redox homeostasis, and viral infections: implications for SARS-CoV-2 (COVID-19).Free radical research · 2021Review
- G6PD deficiency and severity of COVID19 pneumonia and acute respiratory distress syndrome: tip of the iceberg?Annals of hematology · 2021Article
- A Southeast Asian Perspective on the COVID-19 Pandemic: Hemoglobin E (HbE)-Trait Confers Resistance Against COVID-19.Medical science monitor basic research · 2021Article
- Traveling for heart transplantation and returning with COVID-19: a logistical, clinical, and pharmacotherapeutic challenge from the Middle East.Drugs & therapy perspectives : for rational drug selection and use · 2021Article
- Glucose-6-phosphate dehydrogenase deficiency and SARS-CoV-2 mortality: Is there a link and what should we do?Clinical biochemistry · 2020Article
- Structure and functions of cellular redox sensor HSCARG/NMRAL1, a linkage among redox status, innate immunity, DNA damage response, and cancer.Free radical biology & medicine · 2020Review
- Can a metabolism-targeted therapeutic intervention successfully subjugate SARS-COV-2? A scientific rational.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2020Review
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucose-6-phosphate dehydrogenase (G6PD)-deficient cells are highly susceptible to viral infection. This study examined the mechanism underlying this phenomenon by measuring the expression of antiviral genes-tumor necrosis factor alpha (TNF-α) and GTPase myxovirus resistance 1 (MX1)-in G6PD-knockdown cells upon human coronavirus 229E (HCoV-229E) and enterovirus 71 (EV71) infection. Molecular analysis revealed that the promoter activities of TNF-α and MX1 were downregulated in G6PD-knockdown cells, and that the IκB degradation and DNA binding activity of NF-κB were decreased. The HSCARG protein, a nicotinamide adenine dinucleotide phosphate (NADPH) sensor and negative regulator of NF-κB, was upregulated in G6PD-knockdown cells with decreased NADPH/NADP⁺ ratio. Treatment of G6PD-knockdown cells with siRNA against HSCARG enhanced the DNA binding activity of NF-κB and the expression of TNF-α and MX1, but suppressed the expression of viral genes; however, the overexpression of HSCARG inhibited the antiviral response. Exogenous G6PD or IDH1 expression inhibited the expression of HSCARG, resulting in increased expression of TNF-α and MX1 and reduced viral gene expression upon virus infection. Our findings suggest that the increased susceptibility of the G6PD-knockdown cells to viral infection was due to impaired NF-κB signaling and antiviral response mediated by HSCARG.
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