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Objective <p>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.</p> Methods <p>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 (&lt; 35 vs. ≥35 years) and multivariate adjustment for viral load (Ct ≤ 30).</p> Result <p>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 <i>P</i> = 0.001). Age ≥ 35 years independently increased HSIL + risk (OR = 2.16, 95% CI:1.62–2.88, <i>P</i> = 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, <i>P</i> = 0.001). Multiple infections did not increase risk for genotypes 16/18/33/35/52/56/58/68 versus single infections, except for HPV51 (<i>P</i> = 0.01).</p> Conclusion <p>Genotype 16 demonstrates the strongest oncogenic potential, with pathogenic hierarchy: 16 &gt; 58 &gt; 18 &gt; 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.</p> Clinical trial number <p>Not applicable.</p>

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Clinical study on the pathogenic risks of different genotypes of high-risk HPV infection and multiple infections

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月6日

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  • Meiyu Song,
  • Minhong Mao,
  • Huirong Zhao,
  • Chen Chen

摘要

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.