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Objective <p>The study aims to investigate the correlation between the viral loads of HPV16/18 and 16 other high-risk HPV types (designated as non-16/18 group) and the severity of cervical lesions, and to develop a HSIL+ risk prediction model to furnish evidence for pragmatic clinical triage and precision management strategies.</p> Methods <p>A retrospective analysis was performed on the data from 331 HR-HPV-positive patients collected between July 2025 and January 2026. Using a semi-quantitative hybrid capture-chemiluminescence platform,The viral loads of HPV16/18 and non-16/18 group were measured, and patients were categorized into normal, LSIL, HSIL, and cervical cancer groups based on pathological findings.</p> <p><?noindent??>Multivariate logistic regression analysis was employed to examine the associations among viral load, HPV subtypes, age, and lesion severity, and a HSIL+ prediction nomogram was constructed.</p> Results <p>The prevalence of HPV16/18 infection escalated with increasing lesion severity (HSIL: OR=6.50; cervical cancer: OR=23.28), demonstrating a pattern of “continuous augmentation”. Conversely, the viral load of non-16/18 group increased during the LSIL and HSIL stages but declined in the cancer stage, exhibiting a pattern of “early involvement followed by later attenuation”. While single non-16/18 group infections demonstrated early warning value, HPV16/18 types and medium to high viral loads were identified as independent risk factors for HSIL+. The nomogram underwent Bootstrap validation and yielded an AUC of 0.763, indicating satisfactory calibration.</p> Conclusion <p>This study comprehensively analyzed the pathogenic features of viral loads associated with HPV16/18 and other high-risk subtypes, elucidating the lesion patterns of distinct subtypes. While HPV16/18 acts as the principal persistent driver, the high viral load of the non-16/18 group provides a critical "window-of-opportunity" indication during the precancerous phase. A pragmatic HSIL+ risk-stratification nomogram was devised to serve as an accessible clinical aid for the early identification of high-risk lesions, thereby optimizing real-world personalized management.</p>

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Correlation between high-risk Human Papillomavirus (HPV) viral load and cervical lesions across different subtypes, along with the development of a clinical prediction model

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年8月4日

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  • Hongyi Chen,
  • Chenxi Yang,
  • Hongwei Wang

摘要

Objective

The study aims to investigate the correlation between the viral loads of HPV16/18 and 16 other high-risk HPV types (designated as non-16/18 group) and the severity of cervical lesions, and to develop a HSIL+ risk prediction model to furnish evidence for pragmatic clinical triage and precision management strategies.

Methods

A retrospective analysis was performed on the data from 331 HR-HPV-positive patients collected between July 2025 and January 2026. Using a semi-quantitative hybrid capture-chemiluminescence platform,The viral loads of HPV16/18 and non-16/18 group were measured, and patients were categorized into normal, LSIL, HSIL, and cervical cancer groups based on pathological findings.

Multivariate logistic regression analysis was employed to examine the associations among viral load, HPV subtypes, age, and lesion severity, and a HSIL+ prediction nomogram was constructed.

Results

The prevalence of HPV16/18 infection escalated with increasing lesion severity (HSIL: OR=6.50; cervical cancer: OR=23.28), demonstrating a pattern of “continuous augmentation”. Conversely, the viral load of non-16/18 group increased during the LSIL and HSIL stages but declined in the cancer stage, exhibiting a pattern of “early involvement followed by later attenuation”. While single non-16/18 group infections demonstrated early warning value, HPV16/18 types and medium to high viral loads were identified as independent risk factors for HSIL+. The nomogram underwent Bootstrap validation and yielded an AUC of 0.763, indicating satisfactory calibration.

Conclusion

This study comprehensively analyzed the pathogenic features of viral loads associated with HPV16/18 and other high-risk subtypes, elucidating the lesion patterns of distinct subtypes. While HPV16/18 acts as the principal persistent driver, the high viral load of the non-16/18 group provides a critical "window-of-opportunity" indication during the precancerous phase. A pragmatic HSIL+ risk-stratification nomogram was devised to serve as an accessible clinical aid for the early identification of high-risk lesions, thereby optimizing real-world personalized management.