ArticleCentral-European journal of immunology2025
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Article in Central-European journal of immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: The progression of fungal co-infection with COVID-19 depends on the patient's genetic innate immunity. Our goal is to understand the connection between the single nucleotide polymorphisms (SNPs) rs5743708 and rs16910526 in the toll-like receptor 2 (TLR2) and dectin-1 (CLEC7A) genes, respectively, and fungal infection in COVID-19 patients. Material and methods: This study assessed the SNPs rs5743708 from the TLR2 gene and rs16910526 from dectin-1 by Sanger sequencing. Two groups of COVID-19 patients participated in this study: 110 COVID-19 patients free from fungal infection (COVID-19 FFI), and 77 COVID-19 patients with fungal infection (COVID-19 WFI). Results: The AG genotype of the TLR2 SNP rs5743708 showed no significant association with fungal infection in COVID-19 compared to the AA genotype. However, the GG genotype and G allele were significantly associated with decreased vulnerability to fungal co-infections. Similarly, regarding the dectin-1 SNP rs16910526, the TG genotype did not show a significant association with fungal infection compared to the TT genotype, but the GG genotype and G allele were significantly related to decreased susceptibility to fungal co-infections in COVID-19. The TLR2 protein levels in the serum of COVID-19 patients with GG genotypes of TLR2 rs5743708 were elevated. Variations in the dectin-1 genotypes (specifically GG genotype) can also raise the levels of dectin-1 serum protein. Conclusions: The relationship between TLR2 rs5743708 and dectin-1 rs16910526 SNPs and susceptibility to fungal infection in COVID-19 patients was found to be significant, highlighting the im- portance of investigating their connection to infection progression for personalized patient care. The variation in genotypes also affects the levels of corresponding serum TLR2 and dectin-1.
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