ArticleHuman genomics2026
Genetic variations in AAK1 and ADAM17 associated with circulatory cytokines changes influence COVID-19 susceptibility and severity.
Article in Human genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
backgroundThe interplay between genetic factors and COVID-19 susceptibility and severity underscores the critical roles of genetic variations in the responses to the virus. Specifically, genetic variations in genes such as AAK1 and ADAM17 may influence the molecular pathways that determine how the virus enters cells and how the immune system responds, thereby affecting disease outcomes. Identifying these potential genetic variants clarifies individual responses to infectious diseases and helps aid in developing effective targeted therapeutic strategies.
methodsWe performed targeted next-generation sequencing focusing on specific single-nucleotide variants (SNVs) in AAK1, ADAM17, and CD209 genes, which are implicated in the entry of SARS-CoV-2 into host cells. The study was conducted in a Middle Eastern cohort, comprising 96 COVID-19 patients with varying disease severities and 69 healthy controls. The correlation between the prevalence of the investigated genetic variants and the serum level of inflammatory cytokines within the studied cohort was also evaluated.
resultsOur analysis revealed statistically significant differences in genetic variants between COVID-19 patients and healthy controls. Notably, a 5'UTR variant, rs12692386: chr2:9695906, A > G, in the ADAM17 gene showed a significant association (p = 0.039). Additionally, two variants in the AAK1 gene, an intronic variant chr2:69732672, C > A (p = 0.029) and a missense variant rs1275698668: chr2:69747984, G > C (p = 0.017), were identified, suggesting their potential role in influencing disease susceptibility and severity. The gender-stratified analysis between the two groups showed a significant difference in the AAK1-SNV-rs1275698668 (p = 0.027) in female susceptibility, suggesting a protective effect against SARS-CoV-2 infection. The AAK1-SNV-rs1275698668 showed a significant difference between the three severity groups (p = 0.045). Prediction in-silico tools suggest that 2:g.69747984G > C and 2:g.9,695,906 A > G have potential functional/regulatory impacts on the ADAM17 and AAK1 genes, respectively. Moreover, different correlation patterns between the identified genetic variants and inflammatory cytokine levels (including CD40 ligand, IL-1b, GM-CSF, and IL-4) were observed in COVID-19 patients.
conclusionsOur findings suggest potential genetic biomarkers in AAK1 and ADAM17 genes that could affect the disease severity and circulating cytokine levels in COVID-19 patients.
Indexed as
Identifiers
What Socratic holds
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.