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TLR7 polymorphisms are associated with COVID-19 susceptibility and severity
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Journal Article
TLR7 polymorphisms are associated with COVID-19 susceptibility and severity
2026
Overview
SARS-CoV-2 infection causes an innate immune response that is activated through pattern-recognition receptors (PRRs), including Toll-like receptors (TLRs) and retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs). Endosomal TLR7/8 detects viral ssRNA, while TLR3 also recognizes dsRNA formed during viral replication. Both RIG-I and MDA5 recognize SARS-CoV-2 RNA in the cytoplasm of infected cells. PRR pathways recruit essential downstream adapter proteins to induce type I interferons (IFNs) and inflammatory cytokines. While genetic variations in host
may influence SARS-CoV-2 infection, immune response, and COVID-19 severity, their specific role in triggering these processes remains unclear. This study analyzes the frequency of specific polymorphisms within
genes in COVID-19 patients to evaluate their impact on disease severity.
We genotyped ten
polymorphisms in 261 individuals, including 166 patients hospitalized for COVID-19, and evaluated their associations with clinical parameters and serum cytokine profiles. Single-nucleotide polymorphisms (SNPs) of
(rs3775290 and rs3775291),
(rs179008, rs3853839, and rs5741880),
(rs3764879 and rs3764880),
rs1990760, and
rs73479410 were genotyped using qPCR allelic discrimination, while
rs3775296 was analyzed by PCR-RFLP. Cytokine concentrations were quantified using MILLIPLEX Magnetic Bead Panels and Luminex xMAP technology.
In this case-control study, the recessive G/G genotype of the
rs3853839 SNP was associated with an increased risk of hospitalization. The presence of at least one recessive T allele for the
rs179008 SNP was associated with lower cytokine levels (IP-10, IL-10, TNF-α) and a decreased risk of severe symptoms in hospitalized patients.
Our findings suggest that the
rs3853839 SNP may represent a genetic risk factor for severe COVID-19, whereas the missense
rs179008 SNP (Q11L) may contribute to less severe symptoms among these patients.
Publisher
Frontiers Media SA,Frontiers Media S.A
Subject
/ Adult
/ Aged
/ Chronic obstructive pulmonary disease
/ COVID-19
/ cytokine
/ DEAD Box Protein 58 - genetics
/ Diabetes
/ Diarrhea
/ Dyspnea
/ Female
/ Fever
/ Genetic Predisposition to Disease
/ Genotype
/ Humans
/ Interferon-Induced Helicase, IFIH1 - genetics
/ Male
/ Polymorphism, Single Nucleotide
/ Proteins
/ Respiratory distress syndrome
/ Restriction fragment length polymorphism
/ RLR
/ Sepsis
/ Severe acute respiratory syndrome coronavirus 2
/ Single-nucleotide polymorphism
/ TLR
/ Toll-Like Receptor 3 - genetics
