Vulvovaginal candidiasis (VVC) is a prevalent vaginal infection predominantly attributed to Candida albicans. A considerable proportion of women experience more than three episodes of VVC annually, a condition referred to as recurrent vulvovaginal candidiasis (RVVC). It is estimated that RVVC affects more than 130 million women globally each year and has a substantial negative impact on their quality of life, resulting in physical discomfort, psychological distress, and social stigma. Nevertheless, not all individuals who develop VVC progress to RVVC, suggesting that genetic variation may play a critical role in host susceptibility. The present review aims to evaluate the associations between genetic predispositions—specifically polymorphisms in Toll-like receptors 2 and 4 (TLR2, TLR4)—and RVVC. TLRs are essential for detecting pathogen-associated molecular patterns (PAMPs) and initiating immune responses. During RVVC episodes, Candida undergoes a reversible transition from the yeast form to the hyphal form, resulting in alterations in surface PAMPs, which are subsequently recognized by innate immune receptors expressed on vaginal epithelial cells. Polymorphisms in these receptors may modulate individual susceptibility to RVVC. This review examines the literature on the impact of specific polymorphisms in TLR2 and TLR4 on fungal recognition and infection. Furthermore, the interactions between TLRs and other elements of the innate immune system have also been explored. A deeper understanding of how genetic variability in immune receptors influences infection susceptibility could pave the way for personalized therapeutic strategies for RVVC, potentially involving immunomodulatory agents or antifungal treatments tailored to an individual’s genetic profile.

Recurrent vulvovaginal candidiasis (RVVC) affects 5–8% of women of reproductive age. Host genetic factors, particularly single nucleotide polymorphisms (SNPs) in Toll-like receptors (TLRs), may influence RVVC susceptibility by impairing vaginal mucosal antifungal immunity. The aim of this study was to assess the effect of SNPs in genes encoding TLRs on RVVC susceptibility. Τhe distribution of TLR2 Arg753Gln and TLR4 Asp299Gly/Thr399Ile polymorphisms in Greek women, including RVVC (n = 63), first-episode VVC (n = 37), Gardnerella vaginalis vaginitis (GV, n = 36) patients, and healthy controls (n = 61), was investigated using TaqMan SNP genotyping. Genotype and allele frequencies were analyzed under allelic and dominant models, with odds ratios (ORs), 95% confidence intervals (CIs), and linkage disequilibrium assessed. TLR4 Asp299Gly and Thr399Ile heterozygotes were significantly more frequent in RVVC patients compared with controls and affected RVVC susceptibility (OR: 5.57, 95% CI: 1.17–26.56, p: 0.0172; OR: 4.92, 95% CI: 1.02–23.78, p: 0.0306, respectively). No associations were observed for TLR2 Arg753Gln or for any SNP with GV or first-episode VVC. TLR4 variants co-segregated, indicating a haplotype effect. TLR4 haplotypes, rather than TLR2 polymorphism, confer increased RVVC susceptibility, supporting a genetically distinct, mucosal immunity-driven pathogenesis. Larger, ethnically diverse studies with functional assays are warranted to validate these findings and guide personalized prevention and treatment strategies.

Chlamydia is the most common sexually transmitted infection (STI) worldwide. In 2020, the global prevalence was estimated to be 4.0% among women and 2.5% among men aged 15 to 49 years. In more than 80% of cases, the infection is asymptomatic, thereby increasing the risk of subsequent infections. Complications in women can include chronic pain, pelvic inflammatory disease, and an increased risk of ectopic pregnancies. Chlamydia trachomatis (CT) infections can be diagnosed using several techniques, including cell culture, immunofluorescence, enzyme immunoassays, and polymerase chain reaction (PCR). PCR is regarded as the gold standard for screening and detection of CT. We conducted a three-year retrospective study from January 2022 to December 2024, collecting 4241 cervicovaginal swab samples from outpatient gynecology patients. The overall prevalence of CT in our study was 2.02%. An increase in CT detection during the study period was observed: from 24 cases (1.7%) in 2022 to 30 cases (2%; p = 0.64) in 2023 and 32 cases (2.35%; p = 0.26) in 2024. The highest proportion of cases was observed in the 20–24 and 25–34 age groups. Notably, 7 out of 10 cases were asymptomatic. Risk factors for chlamydial infections include behavioral factors, such as having multiple sexual partners and engaging in risky sexual practices, as well as social and lifestyle influences.

Vulvovaginal candidiasis (VVC) is a prevalent vaginal infection predominantly attributed to Candida albicans. A considerable proportion of women experience more than three episodes of VVC annually, a condition referred to as recurrent vulvovaginal candidiasis (RVVC). It is estimated that RVVC affects more than 130 million women globally each year and has a substantial negative impact on their quality of life, resulting in physical discomfort, psychological distress, and social stigma. Nevertheless, not all individuals who develop VVC progress to RVVC, suggesting that genetic variation may play a critical role in host susceptibility. The present review aims to evaluate the associations between genetic predispositions—specifically polymorphisms in Toll-like receptors 2 and 4 (TLR2, TLR4)—and RVVC. TLRs are essential for detecting pathogen-associated molecular patterns (PAMPs) and initiating immune responses. During RVVC episodes, Candida undergoes a reversible transition from the yeast form to the hyphal form, resulting in alterations in surface PAMPs, which are subsequently recognized by innate immune receptors expressed on vaginal epithelial cells. Polymorphisms in these receptors may modulate individual susceptibility to RVVC. This review examines the literature on the impact of specific polymorphisms in TLR2 and TLR4 on fungal recognition and infection. Furthermore, the interactions between TLRs and other elements of the innate immune system have also been explored. A deeper understanding of how genetic variability in immune receptors influences infection susceptibility could pave the way for personalized therapeutic strategies for RVVC, potentially involving immunomodulatory agents or antifungal treatments tailored to an individual’s genetic profile.