Authors
Abir Azri, Duaa A Althumairy, Hager Memni, Mohammed A Almalki, Ikbel Hadj Hassine, Noureddine Chatti, Jawhar Gharbi, Manel Ben M'hadheb
Published in
Viruses. Volume 18. Issue 10. Oct 16, 2026. Epub Oct 16, 2026.
Abstract
The IFNAR2 gene encodes an essential component of the type I interferon receptor, which is essential for antiviral defense. It has been proven that the severity of COVID-19 may be influenced by the genetic variants in IFNAR2; however, the results are inconclusive in the African cohorts. Thus, in this study, we investigate the association between three IFNAR2 SNPs and the critical form of COVID-19 in the Tunisian population. A total of 413 COVID-19 patients classified as hospitalized with critical illness (ICU) (n = 46) and non-hospitalized (n = 367) are included. Genotyping of three IFNAR2 polymorphisms (rs1051393, rs2236757, rs9984273) was performed using Taq Man RT-PCR assays. rs2236757 (OR = 0.31, 95% CI: 0.16-0.60), p = 4 × 10-4) and rs9984273 (OR = 0.41, 95% CI: 0.22-0.76, p = 0.0055) were associated with COVID-19 severity with a potential protective effect. However, rs1051393 did not show a significant association with disease severity. Additionally, exploratory haplotype analysis suggested a possible protective association for the TAC haplotype (OR = 0.11, 95% CI: 0.02-0.86, p = 0.036), based on a very small number of carriers and not significant after correction for multiple testing. The GAC haplotype, absent from ICU patients, yielded a continuity-corrected OR of 0.03 (95% CI [0.002-0.53]); this estimate rests on a zero cell and is hypothesis-generating only. These preliminary findings, obtained from a single-center cohort with a limited number of critically ill patients, warrant replication in larger, independent, and multicentric populations.
PMID:
42944068
Bibliographic data and abstract were imported from PubMed on 27 Oct 2026.
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