Analysis of HPV Genotype Distribution, Viral Load Profiles, and Their Relationship With Cervical Pathology Among Women in Samarkand Region (2023-2025)

Abstract Introduction: Persistent infection with high-risk oncogenic human papillomavirus (HPV) is the primary cause of cervical cancer development. Objective To evaluate the prevalence of various HPV genotypes, describe genotype-specific viral load patterns, and determine their relationship with patient age and cervical cytological changes among women in the Samarkand region. Methods In a cross-sectional study (2023–2025), cervical epithelial samples from 535 women (aged 19–56 years) were analyzed. Genotyping of 21 HPV types and quantification of viral load (expressed in \(\:\text{l}\text{g}\) copies of DNA/10⁵ cells) were performed using real-time PCR. Cytological status was classified according to The Bethesda System (TBS, 2014) in cohorts with monoinfection (n = 73) and mixed infection (n = 20). Results Out of 116 HPV-positive cases, HPV 16 was unconditionally dominant (24%). An atypically low prevalence of HPV 18 (3%) was observed alongside a high detection rate of non-vaccine types: HPV 56 (6%), 51 (5%), and 58 (4%). No statistically significant correlation was found between patient age and viral load (p > 0.05). A significant overall association was revealed between HPV genotype and cytological status (χ²=97.06; df = 68; p = 0.012). HPV 58 demonstrated the highest pathogenetic potential (OR = 12.11; 80% of cases were ASC-US, 20% were ASC-H) and was never detected in normal cytology (NILM). No direct linear correlation was found between viral load level and lesion severity: peak loads were recorded in NILM cases, whereas the only severe case (HSIL, associated with HPV 68) presented with a low viral load (2.7 lg copies/10⁵ cells). Conclusion The regional epidemiological profile is determined by the dominance of HPV 16 and a high circulation of high-risk non-vaccine strains (56, 51, 58). Viral load exhibits immense genotype-specific variability and does not directly correlate with the severity of cytological changes, highlighting the necessity of integrating multi-genotype PCR testing and cytological screening.