A retrospective study on the distribution and pathogenic risks of potential high-risk HPV genotypes in cervical lesions among Chinese women: Evidence from the largest academic women’s hospital in China

A retrospective study on the distribution and pathogenic risks of potential high-risk HPV genotypes in cervical lesions among Chinese women: Evidence from the largest academic women’s hospital in China | Authorea try { document.documentElement.classList.add('js'); } catch (e) { } var _gaq = _gaq || []; _gaq.push(['_setAccount', 'G-8VDV14Y67G']); _gaq.push(['_trackPageview']); (function() { var ga = document.createElement('script'); ga.type = 'text/javascript'; ga.async = true; ga.src = ('https:' == document.location.protocol ? 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Data may be preliminary. 8 May 2025 V1 Latest version Share on A retrospective study on the distribution and pathogenic risks of potential high-risk HPV genotypes in cervical lesions among Chinese women: Evidence from the largest academic women’s hospital in China Authors : Xie Yan , Cong Qing , Zhong Fangfang , and Xiang Tao 0000-0002-1052-118X [email protected] Authors Info & Affiliations https://doi.org/10.22541/au.174671484.48573210/v1 326 views 224 downloads Contents Abstract Information & Authors Metrics & Citations View Options References Figures Tables Media Share Abstract A substantial fraction of cervical cancers arise in women who test negative for the 14 hrHPV types by standard assays, highlighting the need to investigate additional potential high-risk HPV (phrHPV) for screening efficacy. This study is to evaluate the pathogenic potential of phrHPV types—specifically HPV26, 53, 73, and 82—in a Chinese population. A retrospective study was conducted utilizing clinical data and cervical specimens collected from the Obstetrics and Gynecology Hospital of Fudan University between 2017 and 2025. Extended genotyping assays enabled the detection of a comprehensive panel of HPV types. The associations between individual HPV genotypes and the severity of cervical lesions were systematically analyzed. The results showed that in addition to the 14 most prevalent high-risk HPV types, HPV26, 53, 73, and 82 were identified among Chinese women, exhibiting varied degrees of pathogenic potential. Notably, among single infection cases, the incidence rates of CIN2+ were 21.8% for HPV26 and 18.2% for HPV82, with odds ratios of 2.02 (95% CI: 1.33–3.06) and 3.05 (95% CI: 2.13–4.36) compared to HPV-negative cases, respectively. The severity of cervical lesions displayed significant associations with specific HPV types, and these associations were further influenced by the age at infection. Taken together, extended HPV genotyping offers crucial evidence for advancing precision cervical cancer screening strategies in China. Further large-scale, prospective investigations are warranted to confirm and refine optimal genotype targets for population-based cervical cancer screening. A retrospective study on the distribution and pathogenic risks of potential high-risk HPV genotypes in cervical lesions among Chinese women: Evidence from the largest academic women’s hospital in China Xie Yan, MD, PhD 1 , Cong Qing, MD, PhD 1 , Zhong Fangfang, MD 2 , Tao Xiang, MD, PhD 2 Medical Center of Diagnosis and Treatment for Cervical Diseases, Obstetrics and Gynecology Hospital, Fudan University, 419 Fangxie Road, 200011, Shanghai, P.R. China. Department of Pathology, Obstetrics and Gynecology Hospital, Fudan University, 419 Fangxie Road, 200011, Shanghai, P.R. China. Correspondent author: Tao Xiang, Department of Pathology, Obstetrics and Gynecology Hospital, Fudan University, 419 Fangxie Road, 200011, Shanghai, P.R. China, E-mail: [email protected] ABSTRACT A substantial fraction of cervical cancers arise in women who test negative for the 14 hrHPV types by standard assays, highlighting the need to investigate additional potential high-risk HPV (phrHPV) for screening efficacy. This study is to evaluate the pathogenic potential of phrHPV types—specifically HPV26, 53, 73, and 82—in a Chinese population. A retrospective study was conducted utilizing clinical data and cervical specimens collected from the Obstetrics and Gynecology Hospital of Fudan University between 2017 and 2025. Extended genotyping assays enabled the detection of a comprehensive panel of HPV types. The associations between individual HPV genotypes and the severity of cervical lesions were systematically analyzed. The results showed that in addition to the 14 most prevalent high-risk HPV types, HPV26, 53, 73, and 82 were identified among Chinese women, exhibiting varied degrees of pathogenic potential. Notably, among single infection cases, the incidence rates of CIN2+ were 21.8% for HPV26 and 18.2% for HPV82, with odds ratios of 2.02 (95% CI: 1.33–3.06) and 3.05 (95% CI: 2.13–4.36) compared to HPV-negative cases, respectively. The severity of cervical lesions displayed significant associations with specific HPV types, and these associations were further influenced by the age at infection. Taken together, extended HPV genotyping offers crucial evidence for advancing precision cervical cancer screening strategies in China. Further large-scale, prospective investigations are warranted to confirm and refine optimal genotype targets for population-based cervical cancer screening. Keywords: potential high-risk human papillomavirus | cervical intraepithelial neoplasm | infection prevalence | Chinese population | retrospective study 1 | Introduction Cervical cancer ranks among the most prevalent and deadly malignancies affecting women worldwide. Persistent infection with human papillomavirus (HPV), particularly with carcinogenic high-risk genotypes, has been unequivocally established as the principal etiological factor for the development of cervical cancer and its precursors, including cervical intraepithelial neoplasia grade 2/3 (CIN2/3) and adenocarcinoma in situ (AIS). [1, 2] Currently, the most widely employed HPV testing assays in clinical screening target a set of 14 high-risk HPV (hrHPV) types (HPV16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, 68). These genotypes collectively account for over 90% of cervical cancer and high-grade lesion cases in most populations [1]. However, accumulating evidence suggests that a notable proportion—approximately 9.4% to 15.5%—of patients with cervical cancer test negative using these 14-type HPV panels [3, 4]. The etiology of these “HPV-negative” but clinically suspicious cases is multifactorial, encompassing low viral load, limitations in sampling and detection technology, and, importantly, infection with HPV genotypes not included in standard high-risk panels [5]. Recently years have seen increasing attention paid to (phrHPV) types, particularly HPV26, 53, 73, and 82, which have demonstrated non-negligible prevalence rates in specific populations, including Chinese women. For instance, in large eastern China cohorts, the prevalence rates of HPV53, 82, 73, and 26 have been reported at 4.2%, 0.9%, 0.2%, and 1.0%, respectively, occasionally exceeding those of some traditional high-risk types [1]. Evidence from retrospective cohorts suggests that while single infections with phrHPV are occasionally associated with high-grade CIN [1, 6, 7]. The expansion of HPV genotyping to include these additional types could bridge diagnostic gaps, particularly for “HPV-negative” cervical disease, and enhance the sensitivity and comprehensiveness of cervical cancer screening. Although several population studies have preliminarily characterized the distribution and pathogenic risk of these HPV types, systematic assessments of their clinical significance and screening value remain limited, especially the single infection of phrHPV with their follow-up results. As the largest gynecological specialty hospital in China, we previously summarized the HPV genotypes of each histopathological types, including phrHPV, but did not separate single from multiple infection. With more cases in this cohort, we attempted to evaluate the pathogenic potential and epidemiological trends of phrHPV types in a large Chinese population. The insights gained will help clarify their roles in cervical carcinogenesis and inform future screening and preventative strategies tailored to local needs. 2 | Results 2.1 | General characteristics of cases A total of 693,028 cases underwent BMRT HPV genotyping tests. There were 155,946 (22.5%) cases positive for the 18 genotypes of hrHPV and phrHPV; among these, 141,043 (20.4%) cases were positive for hrHPV and 29,037 cases for phrHPV. The mean ages of hrHPV and phrHPV were 41.9±13.5 and 42.7±13.9 (Student- t test, P <0.001). The population infection rates of HPV26, HPV53, HPV73, and HPV82 were 0.12%, 3.5%, 0.33%, and 0.36%, respectively. The infection rate peaks for these four genotypes occurred among women of reproductive age, between 20 and 40 years old. Notably, the prevalence of HPV73 and HPV82 gradually decreased after age 50, the trend of declination in HPV53 was not significant, whereas HPV26 increased rather than decreased after age 50. Compared with the age-specific infection rates of the 14 types of hrHPV within the same age groups, except for HPV53, the peak of positivity for the other 3 types appeared in earlier age categories ( χ 2 test of each phrHPV comparing to hrHPV, P <0.001). (Table 1) 2.2 | The prevalence of single and multiple infections of HPV26, 53, 73, and 82 Approximately half of phrHPV infections were mixed infections, and 97.5% (14,745/15,121) were co-infections with hrHPV, and 2.5% were with other phrHPV. Therefore, considering pathogenic risk, the positivity of phrHPV can be disregarded in most cases. Ranked by the proportion of single-type infections from high to low, the order was HPV53, HPV82, HPV73, and HPV26. Notably, only 33.5% of HPV26 infections were single-type infections, resulting in a single HPV26 population positivity rate of 0.042% (290/693,028). (Table 2) 2.3 | Histological Follow-up of HPV26, 53, 73, and 82 Infections In the database, follow-up biopsy results within 6 months were available for 110 (37.9% of all single-positive cases, same as the following), 4,908 (39.3%), 286 (32.5%), and 302 (28.5%) patients with single infections of HPV26, HPV53, HPV73, and HPV82, respectively. The proportions of CIN2+ found in HPV26 and HPV82 single infections were 21.8% (24/110) and 18.2% (55/302), indicating a higher pathogenic risk for these two types. In contrast, the proportions of CIN2+ for HPV53 and HPV73 single infections were 0.8% (41/4,908) and 2.8% (8/286), suggesting a lower pathogenic risk for these two types. Malignant cases were observed in all four types of single phrHPV infections. Among HPV26-positive cases, there were 6 of 110 (5.5%) cases of invasive squamous cell carcinoma (SCC); among HPV53-positive cases, there were 7 cases of SCC, 1 invasive adenocarcinoma, and 1 small-cell neuroendocrine carcinoma, totally 9 of 4908 (0.18%); among HPV73-positive cases, there was 1 of 286 (0.35%) case of SCC; and among HPV82-positive cases, there were 2 cases of SCC and 2 cases of invasive adenosquamous carcinoma, totally 4 of 302 (1.3%). 2.4 | Risk of CIN2+ associated with HPV26, 53, 73, and 82 infections Since both patient age and infection with different HPV genotypes can influence the prevalence of CIN2+, and HPV infection is often a multiple infection, multivariate logistic regression analysis was used to evaluate the risk of CIN2+ for each phrHPV genotype by assessing the odds ratio ( OR ) for each factor. The risk of developing CIN2+ increased with age: the 30–49 age group had a risk 1.53 times that of those under 30, while the ≥50 age group had a risk of 1.79 times. The risk of CIN2+ in individuals infected with traditional 14 types hrHPV was 3.26 (95% CI : 2.69-3.96) times that of those without infection. For individuals positive for HPV26 and HPV82, the risk of CIN2+ was 2.02 (95% CI : 1.33-3.06) times and 3.05 (95% CI : 2.13-4.36) times higher, respectively, compared to those negative for these types, with statistical significance. Interestingly, HPV53 infection had a protective effect on the development of CIN2+ lesions, with an OR of 0.62 (95% CI : 0.43–0.88). Infection with HPV73 showed no statistically significant impact on the risk of developing CIN2+ lesions. | Discussion This study, based on a large-scale population, systematically evaluated the epidemiological characteristics and pathogenic risks of phrHPV genotypes, including HPV26, HPV53, HPV73, and HPV82, in cervical intraepithelial lesions. The results revealed notable differences in prevalence among these four genotypes. HPV53 displayed a relatively high infection rate in the general population—comparable to or even exceeding several traditional high-risk HPV types—while HPV26, HPV73, and HPV82 remained less common. Specifically, HPV53 ranked among the most prevalent genotypes in multiple cohort studies from China [2, 8, 9]. In contrast, single-type infections with HPV26 and HPV82, though less frequent, were associated with relatively higher rates of CIN2+ lesions, suggesting a greater pathogenic risk for these types [1, 6, 7]. Conversely, despite the high prevalence of HPV53, single infections with HPV53 and HPV73 were linked to significantly lower proportions of CIN2+ lesions, with HPV53 even demonstrating a potential protective effect against progression. These findings were further supported by multivariate logistic regression analysis, which confirmed that HPV26 and HPV82 infections significantly increased the risk of developing CIN2+, whereas HPV53 infection appeared to reduce this risk, and HPV73 showed no statistically significant association with CIN2+. Given the critical role of HPV detection in the classification of cervical cancer and its precursor lesions—including both squamous and glandular origins—the distinction between HPV-dependent and HPV-independent tumors currently relies primarily on HPV test results. However, our findings indicate that a small subset of cases are positive for phrHPV genotypes. When using commercial kits that do not include these genotypes, there is a risk that lesions or cancers may be misclassified as HPV-independent. Furthermore, low viral loads of hrHPV that fall below the assay’s positive threshold can also lead to false-negative results. In our previous investigations of HPV status across diverse types of cervical cancer, the negativity rates for SCC and ADC by the HC2 assay were 14.7% and 33.3%, respectively [2]. When retested using PCR and the Roche Linear Array Kit on corresponding tissue samples, 44.3% of these previously negative cases were found to harbor HPV DNA, with HPV16 being the most prevalent genotype detected [10]. Therefore, differential diagnosis based solely on technical assay results may be misleading. Morphological features can provide valuable adjuncts for distinguishing between HPV-dependent and HPV-independent cancers. For instance, HPV-dependent SCCs tend to exhibit nonkeratinizing morphology, wild-type p53 immunostaining patterns, and are often associated with CIN2/3 in the surrounding tissue. Conversely, HPV-independent SCCs more commonly display keratinizing features, mutant-type p53 immunostaining, and are frequently surrounded by differentiated vulvar intraepithelial neoplasia (dVIN)-like lesions [11]. Consequently, in cases where HPV testing yields negative results, it is imperative that diagnosis be made with caution, integrating both molecular and morphological evidence. In the present study, we demonstrated that HPV26 and HPV82, although exhibiting low prevalence in the general population, possess clear oncogenic potential. Although the majority of HPV26 and HPV82 infections were observed as part of multiple genotype infections, our earlier research—without distinguishing between single and multiple infections—found CIN2+ rates of 14.3% for HPV26 and 16.6% for HPV82 [1], a little lower than those identified in the present study for single infections, which were 21.8% and 18.2%, respectively, indicating a non-negligible carcinogenic risk associated with both genotypes, even in a majority of multiple infection cases, the oncogenic risk were attributable to these specific genotypes rather than to other non HPV16/18 hrHPV types. This underscores the importance of further research to elucidate the role and clinical management of HPV26 and HPV82, particularly in the context of multiple infections. Based on our current findings, as well as corroborating evidence from previous studies—predominantly conducted in Chinese cohorts—these two genotypes warrant inclusion in commercial HPV testing kits for local screening in Chinese population [1, 5-7, 12]. However, the generalizability of this recommendation to other populations should be supported by robust, population-specific investigations, due to possible regional variations in genotype distribution and associated risk. Based on the current study, HPV53 and HPV73 do not confer substantial clinical significance for screening purposes, particularly with regard to HPV53, which demonstrates high prevalence yet an extremely low incidence of CIN2+ lesions [1, 9]. Although invasive cases involving these genotypes have been found, they are better to be explained by co-infections with established hrHPV types with such an undetectable viral titers. For instance, our previous research indicated that the detected viral loads of HPV16, HPV18, and HPV58 in squamous cell carcinoma (SCC) cases were even lower than those in CIN2/3 lesions [13]. Given these findings, routine clinical detection of HPV53 and HPV73 may result in unnecessary overtreatment or increased psychological burden for patients, underscoring the need for more precise, evidence-based HPV genotyping strategies. This study has several limitations. As a retrospective analysis, the cohort was neither systematically nor prospectively enrolled, and the majority of patients underwent colposcopic evaluation due to clinical symptoms or abnormal cytology findings rather than through routine population-based HPV screening. Additionally, the study population was largely derived from a single, high-volume academic hospital in Eastern China. This hospital-based, primarily urban and referral-oriented setting likely enriches for higher-risk individuals, contributing to referral bias and limiting the generalizability of the findings to the wider community or rural populations. 4 | Materials and Methods 4.1 | Study design and sample source This study was conducted as a retrospective data analysis using archival records from the Department of Pathology at the Obstetrics and Gynecology Hospital of Fudan University (OGHFU), the largest academic women’s hospital in China and a major referral center serving a diverse population across Shanghai, neighboring provinces, and nationwide. The study period covered specimens collected between 2017 and 2025. HPV testing were performed by either Roche cobas 4800 (Roche Molecular Systems, Inc., CA, USA) or BioPerfectus Multiplex Real-Time PCR (BMRT) 21-genotype assay (Jiangsu BioPerfectus Technology Co., Taizhou, China) were available during the study period, only cases tested by the BMRT 21-genotype assay were included in the analysis. The study protocol received approval from the Institutional Review Board of OGHFU. 4.2 | HPV testing HPV testing was performed utilizing the BMRT assay, using PCR primers and corresponding TaqMan probes designed to detect each of the 21 most prevalent HPV types, including 14 hrHPV (HPV16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, 68) and potential hrHPV (phrHPV) genotypes (HPV26, 53, 73 and 82) and 3 low risk HPV (lrHPV) genotypes (HPV6, 11 and 81, The kit was designed as 3 HPV types in one amplicon, with human TOP3 gene as internal control. The experimental procedure was performed on an ABI Prism 7500 Fast Dx System (Thermo Fisher Scientific, Waltham, MA, USA) according to the kit manufacturer’s instructions. Final results were expressed as negative or viral loads per one cell for each positive genotype. Only qualification results of either negative or positive for each genotypes were adopted in this study. 4.3 | Histopathological diagnosis Histopathologic diagnostic specimens included cervical biopsies, endocervical curettage, loop electrosurgical excision procedures (LEEP)/cone biopsies, or hysterectomies performed within 6 months of HPV testing. Histopathologic results were categorized into 3 general groups: 1) Negative 2) Cervical intraepithelial neoplasia 1 (CIN1) and 3) Cervical intraepithelial neoplasia 2 and more severe lesions (CIN 2+), including CIN2/3, squamous cell carcinoma, adenocarcinoma in situ (AIS), and endocervical adenocarcinoma. Diagnostic interpretations were confirmed either with immunohistochemical stains for p16/Ki-67 or were reviewed by a second pathologist. In patients with more than one tissue sample or more than one biopsy during this period, the most abnormal diagnosis was recorded. 4.4 | Statistical analysis All samples were classified by age groups and HPV infection genotypes (traditional 14 types vs. target 4 phrHPV types). Descriptive statistics were used to calculate the infection rates of each HPV genotype and the proportions of single and multiple infections within each age group. The Student- t test was used to compare ages. The Pearson χ 2 test was used to compare statistical differences among groups. Logistic regression models were constructed with CIN2+ as the dependent variable and age, single and combined infections of HPV26, HPV53, HPV73, and HPV82 as independent variables to calculate the odds ratio ( OR ), 95% confidence interval ( CI ), and P value. Two-tailed P < 0.05 was considered statistically significant. References: 1. Zhong F, Li Z, Sun Y, et al. HPV genotyping of cervical histologic specimens of 61, 422 patients from the largest women hospital in China . Front Oncol . 2023. 13: 1161631. 2. Tao X, Griffith CC, Zhou X, Wang Z, Yan Y, Li Z, Zhao C. History of high-risk HPV and Pap test results in a large cohort of patients with invasive cervical carcinoma: experience from the largest women’s hospital in China . Cancer Cytopathol . 2015. 123(7): 421-7. 3. de Sanjose S, Quint WG, Alemany L, et al. Human papillomavirus genotype attribution in invasive cervical cancer: a retrospective cross-sectional worldwide study . Lancet Oncol . 2010. 11(11): 1048-56. 4. Saraiya M, Unger ER, Thompson TD, et al. US assessment of HPV types in cancers: implications for current and 9-valent HPV vaccines . J Natl Cancer Inst . 2015. 107(6): djv086. 5. Tao G, Yaling G, Zhan G, Pu L, Miao H. Human papillomavirus genotype distribution among HPV-positive women in Sichuan province, Southwest China . Arch Virol . 2018. 163(1): 65-72. 6. Chen Z, Li X, Tian D, et al. Study on the clinical characteristics, persistent infection capability and viral load of human papillomavirus type 26 single infection . Virol J . 2024. 21(1): 301. 7. Chen Z, Cheng Q, Zhang X, et al. Study on the clinical characteristics, persistent infection capability, and viral load of human papillomavirus type 82 single infection . Virol J . 2025. 22(1): 68. 8. Jiang L, Tian X, Peng D, et al. HPV prevalence and genotype distribution among women in Shandong Province, China: Analysis of 94,489 HPV genotyping results from Shandong’s largest independent pathology laboratory . PLoS One . 2019. 14(1): e0210311. 9. Chen R, Fu Y, You B, Li Y, Yao Y, Wang X, Cheng X. Clinical characteristics of single human papillomavirus 53 infection: a retrospective study of 419 cases . BMC Infect Dis . 2021. 21(1): 1158. 10. Tao X, Zheng B, Yin F, et al. Polymerase Chain Reaction Human Papillomavirus (HPV) Detection and HPV Genotyping in Invasive Cervical Cancers With Prior Negative HC2 Test Results . Am J Clin Pathol . 2017. 147(5): 477-483. 11. Herrington C, Kim K-R, Kong C, et al. Tumours of the uterine cervix. in WHO Classification of Tumours-Female Genital Tumours , 2020, International Agency for Research on Cancer: Leon. 336-389. 12. Tao X, Austin RM, Zhang H, et al. Histopathologic follow-up and HPV test results with HSIL Papanicolaou test results in China’s largest academic women’s hospital . Cancer Cytopathol . 2017. 125(12): 947-953. 13. Zhong F, Yu T, Ma X, Wang S, Cong Q, Tao X. Extensive HPV Genotyping Reveals High Association between Multiple Infections and Cervical Lesions in Chinese Women . Dis Markers . 2022. 2022: 8130373. Tables: Table 1. Age distribution of distinct phrHPV genotype infection, as well as 14 traditional hrHPV in the same period <20 13 (1.5%) 97 (0.4%) 34 (1.5%) 55 (2.2%) 703 (0.5%) 20-29 225 (26%) 4,566 (18.9%) 647 (28.4%) 882 (35.3%) 28,870 (20.5%) 30-39 180 (20.8%) 6,131 (25.3%) 635 (27.9%) 735 (29.4%) 41,262 (29.3%) 40-49 121 (14%) 4,740 (19.6%) 389 (17.1%) 342 (13.7%) 27,287 (19.3%) 50-59 144 (16.6%) 4,885 (20.2%) 322 (14.2%) 260 (10.4%) 24,842 (17.6%) >=60 183 (21.1%) 3,781 (15.6%) 248 (10.9%) 224 (9%) 18,079 (12.8%) Total 866 (100%) 24,200 (100%) 2,275 (100%) 2,498 (100%) 141,043 (100%) Pearson χ 2 test for comparing each phrHPV with hrHPV, P <0.0001. Table 2. Proportion of single and multiple infection of phrHPV genotypes HPV26 290 (33.5%) 576 (66.5%) 534 (61.7%) 866 HPV53 12,489 (51.6%) 11,711 (48.4%) 11,544 (47.7%) 24,200 HPV73 881 (38.7%) 1,394 (61.3%) 1,316 (57.8%) 2,275 HPV82 1,058 (42.4%) 1,440 (57.6%) 1,351 (54.1%) 2,498 Total 14,718 (49.3%) 15,121 (50.7%) 14,745 (49.4%) 29,839 Pearson χ 2 test for comparing infection alone with multiple infection, P <0.001. Pearson χ 2 test for comparing multiple infection with multiple infection with hrHPV, P =0.371. Table 3. Follow-up of single infection of phrHPV during 6 months after HPV testing Normal CIN1 CIN2+ Total Normal CIN1 CIN2+ Total Normal CIN1 CIN2+ Total Normal CIN1 CIN2+ Total <30 12 (80.0%) 3 (20.0%) 0 (0.0%) 15 351 (66.5%) 175 (33.1%) 2 (0.4%) 528 24 (61.5%) 14 (35.9%) 1 (2.6%) 39 32 (64.0%) 12 (24.0%) 6 (12.0%) 50 30-49 29 (55.8%) 12 (23.1%) 11 (21.2%) 1 52 1,819 (75.5%) 578 (24.0%) 13 (0.5%) 2,410 121 (68.8%) 50 (28.4%) 5 (2.8%) 176 113 (60.8%) 48 (25.8%) 25 (13.4%) 186 >=50 27 (62.8%) 3 (7.0%) 13 (30.2%) 2 43 1,429 (72.5%) 515 (26.1%) 26 (1.3%) 1,970 56 (78.9%) 13 (18.3%) 2 (2.8%) 71 33 (50.0%) 9 (13.6%) 24 (36.4%) 66 Total 68 (61.8%) 18 (16.4%) 24 (21.8%) 110 ,3599 (73.3%) 1,268 (25.8%) 41 (0.8%) 4,908 201 (70.3%) 77 (26.9%) 8 (2.8%) 286 178 (58.9%) 69 (22.8%) 55 (18.2%) 302 Table4. Logistic regression of phrHPV and age predicting CIN2+ during 6 months B S.E. Wald df P OR 95% C.I.for OR Lower Upper Age<30 22.079 2 =50 0.581 0.124 22.027 1 <.001 1.79 1.40 2.28 hrHPV 1.183 0.099 142.327 1 <.001 3.26 2.69 3.96 HPV26 0.703 0.212 10.990 1 0.001 2.02 1.33 3.06 HPV53 -0.485 0.183 7.037 1 0.008 0.62 0.43 0.88 HPV73 -0.159 0.206 0.594 1 0.441 0.85 0.57 1.28 HPV82 1.115 0.183 37.155 1 <.001 3.05 2.13 4.36 Constant -3.920 0.228 296.774 1 0.000 0.020 Information & Authors Information Version history V1 Version 1 08 May 2025 Copyright This work is licensed under a Non Exclusive No Reuse License. Keywords epidemiology genital tract human papillomavirus pathogenesis sexually transmitted disease virus classification Authors Affiliations Xie Yan Obstetrics and Gynecology Hospital of Fudan University Medical Center of Diagnosis and Treatment for Cervical Diseases View all articles by this author Cong Qing Obstetrics and Gynecology Hospital of Fudan University Medical Center of Diagnosis and Treatment for Cervical Diseases View all articles by this author Zhong Fangfang Fudan University View all articles by this author Xiang Tao 0000-0002-1052-118X [email protected] Fudan University View all articles by this author Metrics & Citations Metrics Article Usage 326 views 224 downloads .FvxKWukQNSOunydq8rnd { width: 100px; } Citations Download citation Xie Yan, Cong Qing, Zhong Fangfang, et al. A retrospective study on the distribution and pathogenic risks of potential high-risk HPV genotypes in cervical lesions among Chinese women: Evidence from the largest academic women’s hospital in China. Authorea . 08 May 2025. DOI: https://doi.org/10.22541/au.174671484.48573210/v1 If you have the appropriate software installed, you can download article citation data to the citation manager of your choice. Simply select your manager software from the list below and click Download. For more information or tips please see 'Downloading to a citation manager' in the Help menu . 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