{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,28]],"date-time":"2026-05-28T07:03:22Z","timestamp":1779951802418,"version":"3.53.1"},"reference-count":76,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,5,28]],"date-time":"2026-05-28T00:00:00Z","timestamp":1779926400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>\n                      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\n                      <jats:italic>PRRs<\/jats:italic>\n                      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\n                      <jats:italic>PRR<\/jats:italic>\n                      genes in COVID-19 patients to evaluate their impact on disease severity.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We genotyped ten\n                      <jats:italic>PRR<\/jats:italic>\n                      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\n                      <jats:italic>TLR3<\/jats:italic>\n                      (rs3775290 and rs3775291),\n                      <jats:italic>TLR7<\/jats:italic>\n                      (rs179008, rs3853839, and rs5741880),\n                      <jats:italic>TLR8<\/jats:italic>\n                      (rs3764879 and rs3764880),\n                      <jats:italic>IFIH1<\/jats:italic>\n                      rs1990760, and\n                      <jats:italic>DDX58<\/jats:italic>\n                      rs73479410 were genotyped using qPCR allelic discrimination, while\n                      <jats:italic>TLR3<\/jats:italic>\n                      rs3775296 was analyzed by PCR-RFLP. Cytokine concentrations were quantified using MILLIPLEX Magnetic Bead Panels and Luminex xMAP technology.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      In this case-control study, the recessive G\/G genotype of the\n                      <jats:italic>TLR7<\/jats:italic>\n                      rs3853839 SNP was associated with an increased risk of hospitalization. The presence of at least one recessive T allele for the\n                      <jats:italic>TLR7<\/jats:italic>\n                      rs179008 SNP was associated with lower cytokine levels (IP-10, IL-10, TNF-\u03b1) and a decreased risk of severe symptoms in hospitalized patients.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Our findings suggest that the\n                      <jats:italic>TLR7<\/jats:italic>\n                      rs3853839 SNP may represent a genetic risk factor for severe COVID-19, whereas the missense\n                      <jats:italic>TLR7<\/jats:italic>\n                      rs179008 SNP (Q11L) may contribute to less severe symptoms among these patients.\n                    <\/jats:p>\n                  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