Risk Factors for Human Papillomavirus Positivity in a Tertiary Care Center: A Case-Control Study Incorporating Genotype Distribution, Co-Infection Patterns, and Quantitative Viral Load Analysis.

Background/Objectives: Human papillomavirus (HPV) is the leading cause of cervical cancer and anogenital malignancies, yet its clinical presentation, genotype distribution, co-infection patterns, and viral load are poorly characterised in tertiary-care referrals. This study aimed to identify predictors of HPV positivity and describe genotype, co-infection, and relative viral copy number (Cq values) in this setting. Methods: A retrospective case-control study of 234 patients (97 HPV-positive, 137 HPV-negative) used a 37-genotype qPCR platform at a tertiary-care hospital between January-December 2025. Demographic data, clinical diagnosis categories, genotype profiles, co-infection patterns, and cycle quantification (Cq) values were recorded, and multivariable logistic regression identified independent predictors of HPV positivity. Results: HPV positivity was 41.5% (97/234). Only the clinical diagnosis category independently predicted HPV status. Compared with non-specific presentations, patients with anogenital or viral warts (aOR: 4.25; 95% CI: 1.49-12.14; p = 0.007) and vaginal or vulvar inflammation (aOR: 2.08; 95% CI: 1.19-3.63; p = 0.010) had higher odds of positivity. High-risk genotypes were the second most frequently detected category (40.00% of detections), after low-risk genotypes (48.21%), with HPV-16 leading among high-risk types. Co-infection occurred in 44.3% of HPV-positive patients, mostly involving mixed-risk genotypes. Patients with anogenital warts had lower Cq values than those with urinary tract complaints (p = 0.011), reflecting higher relative viral copy numbers per swab. Conclusions: HPV positivity and relative viral copy number (as approximated by Cq values) tracked more closely with clinical presentation than with demographic background. The dominance of low-risk and high-risk genotypes and the prevalence of mixed-risk co-infections were consistent with the symptomatic profile of the cohort. These findings support interpreting HPV results in light of clinical presentation and extended genotyping with relative viral copy number quantification in tertiary settings.