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Updated: Jan 12, 2026
A Comparative Approach to Characterize the Landscape of Host-Pathogen Protein-Protein Interactions
Published on: July 18, 2013
Clinical study on the pathogenic risks of different genotypes of high-risk HPV infection and multiple infections
Meiyu Song1, Minhong Mao2, Huirong Zhao2
1Department of Obstetrics and Gynecology, Beijing Chaoyang Hospital, Capital Medical University, No. 5, Jingyuan Road, Shijingshan District, Beijing, 100043, China. songmeiyu2016@163.com.
Objective:
To investigate the oncogenic risks of distinct high-risk human papillomavirus (HR-HPV) genotypes and whether multiple infections exacerbate pathogenicity, with analysis of age stratification and viral load impact.
Methods:
Clinical and pathological data from 2,525 patients undergoing colposcopy-directed biopsy for cervical abnormalities (2020-2023) were analyzed. HPV genotyping (18 types) and viral load quantification (Ct-values) were performed using PCR-membrane hybridization. Histopathology (CC/LSIL/HSIL/SCC) was evaluated by blinded experts. Statistical analyses included age stratification (< 35 vs. ≥35 years) and multivariate adjustment for viral load (Ct ≤ 30).
Result:
HR-HPV single-type infections predominated (1,774 cases, 70.26%), with genotype distribution: 16 (17.98%), 52 (10.50%), 58 (7.88%), 53 (4.63%), and 18 (4.55%). Multiple infections occurred in 474 cases (18.77%). Versus HPV-negative/low-risk controls, the highest pathogenic risks were: type 16 (OR = 7.96, 95% CI:5.41-11.71), type 58 (OR = 5.80, 95% CI:3.75-8.99), multiple infections (OR = 5.02, 95% CI:3.42-7.37), type 18 (OR = 4.86, 95% CI:2.95-8.02), and type 35 (OR = 4.07, 95% CI:1.82-9.10) (all P = 0.001). Age ≥ 35 years independently increased HSIL + risk (OR = 2.16, 95% CI:1.62-2.88, P = 0.001), with HPV16/18/35 showing significantly higher ORs in this group. High viral load (Ct ≤ 30) independently predicted HSIL + progression (OR = 2.98, 95% CI:1.92-4.63, P = 0.001). Multiple infections did not increase risk for genotypes 16/18/33/35/52/56/58/68 versus single infections, except for HPV51 (P = 0.01).
Conclusion:
Genotype 16 demonstrates the strongest oncogenic potential, with pathogenic hierarchy: 16 > 58 > 18 > 35. Multiple infections do not synergistically increase risk for dominant genotypes. Age ≥ 35 years and high viral load (Ct ≤ 30) independently elevate cervical lesion severity, supporting their integration into risk-stratified screening protocols.
Clinical Trial Number:
Not applicable.
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