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Background <p>There is a lack of research on the relations among genetic polymorphisms, viral load, adaptability, persistent infection ability, and pathogenicity of human papillomavirus (HPV) type 33. Understanding these relations is crucial for revealing its pathogenic mechanisms and formulating prevention strategies.</p> Methods <p>Exfoliated cervical cells were harvested from female participants in three hospitals located in the southwestern region of China (Guizhou, Sichuan, and Chongqing). Real-time fluorescence PCR technology was used for HPV genotyping and genomic quantification, and Sanger sequencing was used to obtain the gene sequence. then, changing trends in HPV33 detection rates and <i>E6</i>/<i>E7</i> allele frequencies were compared. Positive selection, viral load, pathogenicity, and persistent infection capacity of different <i>E6</i>/<i>E7</i> variants/mutations were analyzed.</p> Results <p>Among 239,743 samples, HPV detection number was 56,681, the HPV33 detection rate was 3.72% (2,110/56,681) among all detected HPV genotypes. Between 2009 and 2023, a downward trend in the HPV33 detection rate was observed. The <i>E6</i> + <i>E7</i> prototype (<i>E6</i> + <i>E7</i> on the same variant is consistent with the reference sequence) was the dominant variant, with a significantly increased allele frequency. This dominant variant showed a significantly higher relative risk in causing persistent infection and cervical diseases (cervical intraepithelial neoplasia and cervical cancer). The viral load in the cervical disease group was significantly higher than that in the lesion-free group, and the viral load in the persistent infection group was significantly higher than that in the viral clearance group. There was no correlation between viral load and major genetic variants/mutations.</p> Conclusions <p>The <i>E6</i> + <i>E7</i> prototype has a significant impact on the pathogenicity and persistent infection capacity of HPV33. Viral load is positively correlated with pathogenicity and persistent infection capacity. It may serve as a biomarker for predicting disease progression during HPV33 screening. Other mechanisms underlying allele replacement require further investigation.</p>

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Study on the detection rate, genetic polymorphism, viral load, persistent infection capacity, and pathogenicity of human papillomavirus type 33

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月26日

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  • Qiongyao Li,
  • Qichen Cheng,
  • Di Tian,
  • Zhengyuan An,
  • Lei Li,
  • Feng Yang,
  • Mingjing Zhang,
  • Ganglin Liu,
  • A. Peixin,
  • Yan Yang,
  • Zuyi Chen

摘要

Background

There is a lack of research on the relations among genetic polymorphisms, viral load, adaptability, persistent infection ability, and pathogenicity of human papillomavirus (HPV) type 33. Understanding these relations is crucial for revealing its pathogenic mechanisms and formulating prevention strategies.

Methods

Exfoliated cervical cells were harvested from female participants in three hospitals located in the southwestern region of China (Guizhou, Sichuan, and Chongqing). Real-time fluorescence PCR technology was used for HPV genotyping and genomic quantification, and Sanger sequencing was used to obtain the gene sequence. then, changing trends in HPV33 detection rates and E6/E7 allele frequencies were compared. Positive selection, viral load, pathogenicity, and persistent infection capacity of different E6/E7 variants/mutations were analyzed.

Results

Among 239,743 samples, HPV detection number was 56,681, the HPV33 detection rate was 3.72% (2,110/56,681) among all detected HPV genotypes. Between 2009 and 2023, a downward trend in the HPV33 detection rate was observed. The E6 + E7 prototype (E6 + E7 on the same variant is consistent with the reference sequence) was the dominant variant, with a significantly increased allele frequency. This dominant variant showed a significantly higher relative risk in causing persistent infection and cervical diseases (cervical intraepithelial neoplasia and cervical cancer). The viral load in the cervical disease group was significantly higher than that in the lesion-free group, and the viral load in the persistent infection group was significantly higher than that in the viral clearance group. There was no correlation between viral load and major genetic variants/mutations.

Conclusions

The E6 + E7 prototype has a significant impact on the pathogenicity and persistent infection capacity of HPV33. Viral load is positively correlated with pathogenicity and persistent infection capacity. It may serve as a biomarker for predicting disease progression during HPV33 screening. Other mechanisms underlying allele replacement require further investigation.