ArticleMolecular psychiatry2022
In COVID-19, NLRP3 inflammasome genetic variants are associated with critical disease and these effects are partly mediated by the sickness symptom complex: a nomothetic network approach.
Article in Molecular psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.
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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.
The trial behind it
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Who cites it
24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 49 citations in OpenAlex.
- Pooled it
- The tryptophan catabolite or kynurenine pathway in COVID-19 and critical COVID-19: a systematic review and meta-analysis.BMC infectious diseases · 2022Pooled it
- Neuroinflammation and Oxidative Stress in Parkinson's Disease, Alzheimer's Disease, and COVID-19: Microglia-Neutrophil Interaction.ACS omega · 2026Review
- The NLRP3 inflammasome as a key pathway in the affective and chronic fatigue symptoms of Long COVID.Journal of translational medicine · 2026Article
- Inflammasome-Related Genetic Polymorphisms as Severity Biomarkers of COVID-19.International journal of molecular sciences · 2024Article
- Impact of NLRP3 gene polymorphisms (rs10754558 and rs10733113) on HPV infection and cervical cancer in southern Chinese population.Infectious agents and cancer · 2023Article
- NLRP3 inflammasome and interleukin-1 contributions to COVID-19-associated coagulopathy and immunothrombosis.Cardiovascular research · 2023Article
- NLRP3, the inflammasome and COVID-19 infection.QJM : monthly journal of the Association of Physicians · 2023Review
- Review
- SARS-CoV-2 drives NLRP3 inflammasome activation in human microglia through spike protein.Molecular psychiatry · 2023Article
- Recuperative herbal formula Jing Si maintains vasculature permeability balance, regulates inflammation and assuages concomitants of "Long-Covid".Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023Article
- MicroRNA 205-5p and COVID-19 adverse outcomes: Potential molecular biomarker and regulator of the immune response.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Article
- Exploring the Role of ACE2 as a Connecting Link between COVID-19 and Parkinson's Disease.Life (Basel, Switzerland) · 2023Review
- Chronic Fatigue, Depression and Anxiety Symptoms in Long COVID Are Strongly Predicted by Neuroimmune and Neuro-Oxidative Pathways Which Are Caused by the Inflammation during Acute Infection.Journal of clinical medicine · 2023Article
- The viral hypothesis in Alzheimer's disease: SARS-CoV-2 on the cusp.Frontiers in aging neuroscience · 2023Review
- Innate and adaptive immunity to SARS-CoV-2 and predisposing factors.Frontiers in immunology · 2023Review
- Inflammasomes: a rising star on the horizon of COVID-19 pathophysiology.Frontiers in immunology · 2023Review
- Inflammasomes during SARS-CoV-2 infection and development of their corresponding inhibitors.Frontiers in cellular and infection microbiology · 2023Review
- Lowered Quality of Life in Long COVID Is Predicted by Affective Symptoms, Chronic Fatigue Syndrome, Inflammation and Neuroimmunotoxic Pathways.International journal of environmental research and public health · 2022Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In coronavirus disease (COVID-19), the nucleotide-binding domain, leucine-rich repeat and pyrin domain-containing protein 3 (NLRP3) inflammasome is activated in response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Acute infections are accompanied by a sickness symptom complex (SSC) which is highly conserved and protects against infections and hyperinflammation. The aim of this study is to delineate the associations of COVID-19, SSC and NLPR3 rs10157379 T > C and NLPR3 rs10754558 C > G variants; and the protective role of SSC in SARS-CoV-2 infection. We recruited COVID-19 patients, 308 with critical, 63 with moderate and 157 with mild disease. Increased SSC protects against SARS, critical disease, and death due to COVID-19. Increasing age, male sex and rs10754558 CG significantly reduce SSC protection. The rs10157379 CT and rs10754558 GG genotypes are positively associated with SARS. Partial Least Squares analysis shows that a) 41.8% of the variance in critical COVID-19 symptoms is explained by SSC and oxygen saturation (inversely associated), inflammation, chest computed tomography abnormalities, increased body mass index, SARS and age (positively associated); and b) the effects of the NLRP3 rs10157379 and rs10754558 variants on critical COVID-19 are mediated via SSC (protective) and SARS (detrimental). SSC includes anosmia and dysgeusia, and maybe gastrointestinal symptoms. In conclusion, intersections among the rs10754558 variant, age, and sex increase risk towards critical COVID-19 by attenuating SSC. NLRP3 variants play an important role in SARS, and severe and critical COVID-19 especially in elderly male individuals with reduced SSC and with increased BMI, hypertension, and diabetes type 2.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.