Background: Chronic periodontitis (CP) is a prevalent infectious disease caused by an interplay between pathogens and immune responses. Gene polymorphisms are among the factors that affect susceptibility to CP. This study aimed to assess the association between CP and single nucleotide polymorphisms (SNPs) of interleukin-10 (IL-10), interleukin 1ß (IL-1ß), and tumor necrosis factor-α (TNF-α) genes. Methods: A total of 87 patients with CP and 89 healthy controls were included in this study. Venous blood samples were obtained, and DNA was extracted and purified. Segments containing the relevant genes were amplified by polymerase chain reaction (PCR). Electrophoresis was performed after restriction fragment length polymorphism (RFLP) to determine genotype and allele frequencies. Results: The CP group showed significantly different allele and genotype frequencies for three out of five SNPs: IL-10 ─ 592 C/A, IL-10 ─ 819 C/T, and IL-1ß + 3954 C/T (p < 0.05). Additionally, the frequency of the TNF-α ─ 857 AA genotype was significantly lower in patients compared with controls (p = 0.034); however, no significant differences were found in allele frequencies (p > 0.05). Logistic regression analysis revealed that carriers of IL-10 ─ 592 A allele and IL-1ß + 3954 T allele are at higher risk of CP (p < 0.001). Allele and genotype frequencies for TNF-α ─ 308 G/A did not differ significantly between patients and controls (p > 0.05). Conclusions: This study showed specific genotypes of IL-10 ─ 592 C/A, IL-10 ─ 819 C/T, IL-1ß + 3954 C/T, and TNF-α ─ 857 G/A SNPs may be associated with an increased risk of CP development.

Background/Objectives: Bitter Taste Receptors (encoded by TAS2R genes) are expressed in mucosal and bronchial epithelia, as well as in immune cells, contributing to defense against airborne pathogens such as SARS-CoV-2. Data on single-nucleotide polymorphisms (SNPs) in TAS2R genes or pseudogenes in COVID-19 are limited. This study examined the association between TAS2R SNPs and COVID-19 infection and seroconversion in European individuals participating in the Canadian Longitudinal Study on Aging. Methods: Data from the Genome-wide Genetic Data, Comprehensive Baseline (version 7.0), Follow-up 2 (version 1.1), COVID-19 Questionnaire Study (4-2020 to 12-2020), and COVID-19 Seroprevalence (Antibody) Study (11-2020 to 7-2021) datasets were accessed. Associations of TAS2R SNPS with COVID-19 infection or seroconversion were determined using logistic regression adjusted for sociodemographics, genetic principal components, smoking, vaccine doses, and chronic medical conditions (diabetes, immune-mediated inflammatory diseases (IMIDs), respiratory disease, and cardiovascular disease). Results: In the COVID-19 Questionnaire Study (N = 14,073), the rs117458236 (C) variant in TAS2R20 showed a trend toward an association with COVID-19 infection (OR = 1.95; 95% Confidence Interval (CI): 0.98, 3.51). In the COVID-19 Antibody Study (N = 8313), the rs2234235(G) variant in TAS2R1 was associated with anti-nucleocapsid (OR = 1.55; CI: 1.06, 2.20) and anti-spike response (OR = 0.74; CI: 0.57, 0.98); the rs2234010(A) variant in TAS2R5 was associated with anti-nucleocapsid (OR = 1.56; CI: 1.08, 2.19); and the rs34039200(A) variant in TAS2R62P was associated with anti-spike (OR = 0.86; CI: 0.77, 0.97). In a subgroup analysis, the rs2234235(G) variant in TAS2R1 was associated with a decreased anti-spike response to infection or vaccination in individuals with IMIDs or respiratory disease and an increased risk of SARS-CoV-2 infection. Conclusions: TAS2R variants are associated with COVID-19 infection and vaccine response. These data may inform personalized management and vaccination strategies.