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Study on the clinical characteristics, persistent infection capability and viral load of human papillomavirus type 26 single infection

Virology Journal volume 21, Article number: 301 (2024) Cite this article

Abstract

Background

Human papillomavirus (HPV) infection is the main cause of cervical cancer. Different types of HPV have varying carcinogenic capabilities, and viral load is one of the key indicators of pathogenicity. Currently, there is a lack of clinical data on HPV26. This study analyzed the clinical characteristics of patients with HPV26 single infection.

Methods

Exfoliated cervical cells were collected for HPV genotyping from women who attended gynecological outpatient clinics or physical examinations. The clinical characteristics of HPV26 single infections in both cross-sectional and follow-up studies were examined, and the association of viral load with HPV26 persistent infection and pathogenicity was investigated.

Results

The HPV26 positive rate among women visiting hospitals for gynecological medical consultation or physical examination was approximately 0.09% (379/435,072). Among the HPV types tested, the detection rate of HPV26 was 0.37% (379/103,608). In the cross-sectional histopathological study of 101 patients with HPV26 single infection, 62.37% (63/101) presented lesion-free. The numbers of patients with cervical intraepithelial neoplasia (CIN) 1, CIN2, and CIN3 were 25, eight, and five, respectively. Cervical cancer was not detected in any patient. 71 patients attended follow-up examinations as well as HPV26 retesting up to two years, during which, 28.57% (6/21) of CIN1 patients have developed into high-grade lesions, and 9.61% (5/52) of lesion-free patients have progressed to CIN stage. The viral load in the CIN group was significantly higher than that in the lesion-free group (p = 0.012). Similarly, the viral load in the persistent infection group was significantly higher than that in the viral-clearance group (p < 0.001).

Conclusions

The pathogenicity of single HPV26 infections is moderate among high-risk types, warranting the inclusion of HPV26 in expanded screening for HPV. High viral load is an important factor in the persistent infection and pathogenicity of HPV26. Viral load is expected to serve as a screening risk factor for persistent infection and disease progression associated with HPV26.

Introduction

Cervical cancer is the fourth most common cancer in women globally, with around 660,000 new cases and 350,000 deaths in 2022 (World Health Organization, 2022) [1]. Generally, up to 90% of cervical cancer cases in developing countries are due to the failure in early cervical cancer screening [1, 2].

Persistent infection with Human Papillomavirus (HPV) is the primary cause of cervical cancer [3]. Over 200 different types of HPV have been identified, around 30 of them are associated with genital infections, classified as low-risk or high-risk types based on their carcinogenicity [4]. Generally, low-risk types include HPV6, 11, 44 and 81, which are associated with benign lesions like genital warts. On the other hand, high-risk types such as HPV16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58 and 59 are usually considered to be able to develop cervical cancer and its precancerous lesion cervical intraepithelial neoplasia (CIN) [5]. HPV genotyping is indispensable in cervical cancer screening, helping in the prediction of cervical cancer and its precancerous lesions progression [6]. Different high-risk types of HPV show significant differences in terms of their carcinogenicity. These high-risk types are classified by The International Agency for Research on Cancer based on the level of evidence associating them with cancer, as “group 1 carcinogenic to humans,” and “probably/possibly carcinogenic to humans (group 2A and group 2B)” [7]. HPV26 is primarily recognized as a high-risk type, with limited evidence in humans linking it to cervical cancer, thus it is categorized as group 2B [7]. Originally, HPV26 was speculated to be a possible oncogenic type based on its phylogenetic relationship with other high-risk HPV types, with the evidence of in vitro molecular experiments [8]. However, clinical data on HPV26 infection remain limited, particularly regarding its viral load.

HPV26 is increasingly being included in the targets of commercial detection assays and preventive vaccines. However, further evidence is needed to support the necessity of HPV26 detection, prevention, and treatment in clinical settings [9,10,11,12]. This study analyzed the infection rate of HPV26 in women visiting hospitals for gynecological medical consultation or physical examination, the pathogenicity of HPV26 single infection, the association between its viral load and pathogenicity and persistent infection. This study aimed to provide intervention-based evidence for the diagnosis and treatment of HPV26.

Methods

Study population and study criteria

(1) From January 1, 2014, to December 31, 2023, exfoliated cervical cells were collected from female participants recruited from the Affiliated Hospital of Zunyi Medical University, Nanchuan Hospital of Chongqing Medical University, Chengdu Huada Hospital, Chongqing Tongnan Maternal and Child Health Hospital, and Chongqing Changshou District Traditional Chinese Medicine Hospital.

(2) Inclusion criteria: Female participants went to the hospitals for gynecological medical consultation or physical examination.

(3) Exclusion criteria: No history of sexual activity, currently menstruating, uterine or vaginal medication/surgery within the past three days, total hysterectomy.

Sample collection

Exfoliated cervical cells were collected by gynecologists using a cervical swab and preserved in commercial cell preservation solution (Chaozhou Kaipu Biochemical Co., Ltd.). Samples were temporarily stored at 4 °C and tested within 24 h of collection.

HPV genotyping

The Human Papillomavirus Nucleic Acid Genotyping Test Kit (National Medical Device Registration Certificate No. 20143402188, Chaozhou Kaipu Biochemical Co., Ltd.) was used for HPV nucleic acid extraction and genotyping. All tests were carried out according to the instructions and using the supporting equipment and consumables recommended in the manual. This kit can detect and genotype 24 major HPV types (high-risk types: 16, 18, 26, 31, 33, 35, 39, 45, 51, 52, 53, 56, 58, 59, 66, 68, 73, 82; low-risk types: 6, 11, 42, 43, 44, 81). Quality control was performed for each batch.

Viral load quantification

The Human Papillomavirus Nucleic Acid Genotyping Test Kit (Fluorescent PCR method) (National Medical Device Registration Certificate No. 20153400364, Jiangsu BioPerfectus Co., Ltd.) was used to determine the HPV26 viral load. This kit can quantitatively detect the concentration of human housekeeping genes while detecting the concentration of HPV genome. The HPV26 viral load per 10,000 cells based on the concentration of the housekeeping genes was calculated [13].

Pathological examination and follow-up

We referred to other studies for cross-sectional and follow-up study methods [14,15,16,17]. Further analysis was carried out for HPV26 single infection positive cases with the inclusion criteria being that HPV genotyping test had been performed within the last six to 24 months, excluding infection with the 15 most common high-risk types (HPV16, 18, 31, 33, 35, 39, 45, 51, 52, 53, 56, 58, 59, 66, 68) and the two most common low-risk types (HPV6, 11). Exclusion criteria: refusal of histopathological biopsy, human immunodeficiency virus infection, taking immunosuppressive drugs, or with more than six sexual partners. All patients were triaged by gynecological colposcopy and/or ThinPrep™ Pap Test PreservCyt (TCT) in the pathology department. Among them, patients with abnormalities in colposcopy and/or cytology underwent histopathological examination, and the grades of cervical lesions were differentiated by histopathology. In this study, we only distinguished among CIN (grades 1–3), cervical cancer, and lesion-free cases.

Patients with high-grade CIN (grade 2 and 3) and cervical cancer were considered disease endpoints and no longer followed up due to the need for treatment. CIN1 and lesion-free female patients were included in follow-up. Follow-up inclusion criteria: HPV26-positive females were informed to undergo re-examination every six months starting from the first examination, and the duration of symptom follow-up lasting between six to 24 months. Follow-up exclusion criteria: surgical treatment, loss to follow-up, and other high-risk HPV infections.

Data analysis

All data were statistically analyzed using SPSS 26.0. The chi-square test was used to compare differences between data sets. Independent sample t-tests were used to assess the significance of differences in mean values between different groups. p < 0.05 was considered statistically significant.

Results

HPV26 positive rate

Among the 435,072 samples tested, 76,821 were positive. And due to the presence of multiple infections, HPV detection number was 103,608. Among them, HPV26 was detected 379 times. The HPV26 positive rate among women visiting hospital and undergoing physical examinations was approximately 0.09% (379/435,072). And among the tested HPV types, the detection rate of HPV26 was 0.37% (379/103,608).

Of the 379 HPV26-positive cases, 129 were single HPV26 infection, of which 104 met the criteria for subsequent analysis. The study flowchart was shown in Fig. 1. Among the 104 patients who met the criteria, three refused tissue biopsy after colposcopy and/or TCT abnormalities, therefore leaving 101 patients (mean age 42.36 ± 11.47 years, age range 23 to 67 years) included in the cross-sectional study. The results of the cross-sectional study showed that 63 cases were lesion-free, 24 cases were CIN1, eight cases were CIN2, and five cases were CIN3.

Fig. 1
figure 1

Study design of HPV26 single infection characteristics. Note: HPV: human papillomavirus; CIN: cervical intraepithelial neoplasia; TCT: ThinPrep™ Pap Test PreservCyt

Full size image

Follow-Up study results

A total of 71 patients completed the follow-up, with an average follow-up time of 10.85 ± 2.81 months and a follow-up time span of 6.63 to 17.93 months. Of the 25 CIN1 patients, three underwent surgery, two were lost to follow-up, and the remaining 20 were included in the analysis as: four maintained CIN1, five progressed to CIN2, one progressed to CIN3, and 10 CIN1 subsided to lesion-free (with HPV26 turned negative). Of the 63 lesion-free patients, two underwent surgery, ten were lost to follow-up, and the remaining 51 were included in the analysis as: four progressed to CIN1, one progressed to CIN2, and 46 remained lesion-free (three had persistent infection, 43 turned negative).

The probability of CIN1 progressed to more severe cervical lesions (30.00%, 6/20) in patients was significantly higher than the lesion-free ones (9.62%, 5/52) (relative risk = 3.12, 95% confidence interval = 1.07–9.07, χ2 = 4.64, p = 0.031).

Viral load study results

The mean logarithmic value of viral load in the CIN group (CIN1 + CIN2 + CIN3) (4.47) (units: log10 copies per 10,000 cells) was significantly higher than that in the lesion-free group (3.91) (t = 2.57, p = 0.012). During follow-up, the mean logarithmic value of viral load in the disease progression group (CIN1 progressing to CIN2 and CIN3, lesion-free progressed to CIN) (4.80) was significantly higher than that in the maintenance or subsided to lesion-free groups (3.99) (t = 2.27, p = 0.027). The detailed information of viral load can be found in Supplementary Material 1.

The mean logarithmic value of viral load in patients with persistent infection (5.24) during follow-up was significantly higher than that in patients with non-persistent infection (3.73) (t = 6.03, p < 0.001).

Discussion

Different HPV types have significant differences in their ability to promote the development of CIN and cervical cancer during persistent infection. Tailored retesting and treatment plans are needed for different types of HPV, and the development of these treatment plans requires a large amount of clinical research data to support them [18]. Due to its low infection rate in the population, obtaining clinical data on HPV26 infection is difficult. Although HPV26 is mentioned in studies on HPV distribution, it is generally not distinguished between single and multiple infections or only small samples are differentiated afterwards. Furthermore, there is a lack of follow-up and viral load studies specific to HPV26 infection. Summarizing the entire study, we utilized a large sample size from multiple centers, analyzing a total of 101 samples with single HPV26 infection for cross-sectional analysis, and obtained follow-up data from 71 patients. Our main study findings indicate that HPV26 has a low infection rate, and although cervical cancer was not found in cases of single infection, a high proportion showed CIN, with a fast disease progression during follow-up. Furthermore, through these samples, we also confirmed that HPV26 viral load is positively correlated with pathogenicity and the ability for persistent infection.

Different HPV types exhibit significant distribution differences in various countries or regions. The development of diagnostic and preventive strategies needs to consider the prevalence of HPV, with high-prevalence and high-carcinogenic types being the focus of detection and prevention [19]. Many studies have specifically reported on the regional characteristics of HPV distribution, primarily focusing on common high-risk types such as 16, 18, 33, 52, and 58 [7, 20, 21]; whereas HPV26, due to its low detection rate, is often described as a rare type with limited analysis [22,23,24]. Similar to other studies, our research found that both the infection rate and detection rate of HPV26 were very low. These studies collectively demonstrate that HPV26 is a relatively rare high-risk type HPV in multiple regions, so its importance is diminished due to its rarity in infections compared to more common predominant types.

Through phylogenetic analysis, HPV26 belongs to the α-5 branch of HPV, classified as a high-risk type. The most common HPV type in α-5 family is HPV51 [17, 25]. Among all common HPV, HPV16 and 18 are considered the two most potent carcinogenic high-risk types, followed by HPV31, 33, 45, 52, 58, and then HPV39, 51, 53, 56, 59 [2, 9]. According to phylogenetic relationships, HPV26 may have a similar carcinogenic ability to HPV51, but the clinical data on the carcinogenic ability of HPV26 in cases of single infection have been lacking due to its rarity. In some cross-sectional studies that did not distinguish between single and multiple infections in HPV infections, even though the sample size of HPV26 infection was small, its distribution in cervical cancer was clearly confirmed [2, 26]. However, different conclusions may be drawn in these studies, for example, HPV26 may be recommended for screening due to its significantly high presence in low-grade squamous intraepithelial lesion [22], or it may warrant attention for its significant induction of high-grade squamous intraepithelial lesion [27]. HPV51 is estimated to account for 1.3% of cervical cancer cases, ranking 10th among all HPV types; while HPV26 is estimated to potentially cause around 0.3% of cervical cancer cases, ranking 15th [28]. A comparable high-risk type is the common HPV53, which is also estimated to cause about 0.3% of cervical cancer cases [28]. We studied the pathogenicity of HPV26 in cases of single infection and found no cases of cervical cancer among 104 cases of single infection. The proportion of cervical cancer and high-grade CIN in cases of single HPV26 infection is much lower than that of HPV16 and 18 [24, 29]; but significantly higher than HPV53, with faster disease progression in cases of single HPV26 infection compared to single HPV53 infection during follow-up [30], indicating that the carcinogenic ability of HPV26 falls within the moderate-risk range among high-risk types. The detection rate of HPV is currently fluctuating, with some types showing significant increases or decreases in detection rates. Despite its lower detection rate, HPV26 is still worth attention due to its considerable pathogenicity among high-risk types.

Viral load is an important indicator of viral infection ability and pathogenicity [31, 32]. A higher viral load may indicate greater difficulty in clearance and potentially stronger persistent infection ability; a higher viral load suggests higher activity of the virus in the patient’s body, with potentially greater pathogenicity. It is widely believed that persistent infection with the same high-risk HPV type is a necessary condition for the development of CIN and cervical cancer [33,34,35,36]. The longer the duration of persistent infection with the same high-risk HPV type, the longer the development of cervical lesions, and the higher the probability of more severe lesions [33,34,35,36]. Therefore, theoretically, HPV viral load may be an important indicator of the persistent infection and pathogenicity of high-risk HPV types. Current studies on HPV viral load and cervical disease show that the viral load of α-9 family HPV types (represented by HPV16, 33, 52, and 58) increases with the severity of cervical disease, with a positive correlation between viral load and more severe cervical lesions; while the viral load of other high-risk HPV types (e.g., HPV18) does not show a significant correlation with more severe cervical lesions [33,34,35,36]. This suggests that there are different correlations between HPV viral load, persistent infection, and pathogenicity, and further research is needed to determine whether viral load of different HPV types can predict disease progression or serve as an auxiliary indicator for assessing the grade of cervical disease. Limited research exists on viral load related to rare high-risk HPV such as type 26. In our study, through a cross-sectional analysis, we confirmed that the HPV26 viral load in the CIN group was significantly higher than in the lesion-free group; and during follow-up, the viral load of HPV26 in the persistent infection group was significantly higher than in the HPV26 clearance group. Viral load-related analysis indicates a positive correlation between HPV26 viral load and disease progression, showing similar characteristics to major high-risk HPV types such as the α-9 family represented by HPV16. Types in the α-5 family, which have close phylogenetic relationships to HPV26, include HPV51, 69, and 82, with their viral loads potentially being positively correlated with persistent infection and pathogenicity.

The low infection rate and limited sample size of single HPV26 infections may introduce bias in the cross-sectional results. Due to the small sample size, we were unable to obtain a sufficient number of CIN2 and CIN3 samples for viral load analysis across different levels of CIN.

Conclusion

Although the infection rate of HPV26 in women undergoing gynecological medical examinations in southwestern China is low, the pathogenicity of single HPV26 infections is moderate among high-risk types, warranting the inclusion of HPV26 in expanded screening for HPV. High viral load is an important factor in the persistent infection and pathogenicity of HPV26. Viral load is expected to serve as a screening risk factor for persistent infection and disease progression associated with HPV26.

Data availability

No datasets were generated or analysed during the current study.

Abbreviations

HPV:

Human papillomavirus

CIN:

Cervical intraepithelial neoplasia

TCT:

ThinPrep™ Pap Test PreservCyt

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Acknowledgements

We sincerely thank the medical staff from the gynecology department, physical examination department and pathology department who contributed to this study, and also express our gratitude to the patients who cooperated with the research.

Funding

This work was supported by grants from the National Natural Science Foundation of China (No.82302527), Guizhou Province “Thousand Talents” Plan (No. xmrc120240204), Affiliated Hospital of Zunyi Medical University Excellent Talents Plan (No. rc220220916), Zunyi Science and Big Data Bureau (Zunyi Science and Technology Cooperation HZ (2023) 239).

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Author notes

  1. Zuyi Chen, Xiaoyang Li and Di Tian equally contributed to this work.

Authors and Affiliations

  1. Department of Laboratory Medicine, Affiliated Hospital of Zunyi Medical University, Zunyi, China

    Zuyi Chen, Di Tian, Jingchi Liu, Xia Bai, Tingting Feng & Shiqi Chen

  2. School of Laboratory Medicine, Zunyi Medical University, Zunyi, China

    Zuyi Chen, Di Tian, Jingchi Liu, Xia Bai, Tingting Feng & Shiqi Chen

  3. General Office, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, Affiliated Cancer Hospital of University of Electronic Science and Technology of China, Chengdu, China

    Xiaoyang Li

  4. Nanchuan Hospital of Chongqing Medical University, Chongqing, China

    Lin Chen

  5. Department of Information, Affiliated Hospital of Zunyi Medical University, Zunyi, China

    Qiongyao Li

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Contributions

ZC, QL, LC and XL conceived and designed the study. ZC, QL, LC, XL, DT, JL, XB, TF and SC performed the experiments. ZC, QL, LC and XL analyzed the data. ZC and QL wrote the paper. All authors read and approved the final manuscript.

Corresponding authors

Correspondence to Lin Chen or Qiongyao Li.

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Ethics approval and consent to participate

The study was approved by the Ethics Committee of Affiliated Hospital of Zunyi Medical University, the approval number was ZYFYLS2018(81). Written informed consents were obtained from all the patients or their guardians. This study was conducted in strict compliance with medical ethics norms.

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The authors declare no competing interests.

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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 21, 301 (2024). https://doi.org/10.1186/s12985-024-02582-w

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Virology Journal

ISSN: 1743-422X