Among the most frequent cancers in females worldwide, cervical cancer ranks the second [10], with an increasing trend in the incidence. Cervical cancer occurrence is related closely with HPV infection, especially HPV 16 and 18 infection caused CIN (cervical intraepithelial neoplasia) of the precancerous stage in most cases [11]. The results of HPV infection were dependent on the genotypes (low-risk or high-risk), 96.6% of ICC (invasive cervical cancer) had relationship with HR-HPV genotype (HPV16, 18, 31, 33, 35, 39, 45, 52, 58, and 59) infections worldwide [12] .
The results of types of HPV from our epidemiological results in Chongqing province, with more than 15 million female population, may provide information about the health practices of the Chinese population. The results of this study reveal a 22.3% overall prevalence of HPV infection in Chongqing province. The infection rate of HPV in Chongqing province was slightly lower than that reported in a previous study in the same region (26.2%)[13], similar to that in the north of Chengdu (23.05%)[14] and Henan (22.8%)[15], noticeably higher than that in Zhejiang (13.3%)[16] and Xinjiang (14.02%)[17], but significantly lower than that in Harbin (36.5%)[18], Fujian (38.3%)[8] and Calabria (31%)[19]. The reason for the differences in HPV prevalence between that reported in our and a previous study [13] may be that most of the participants took part in the screening in the previous study because of the discomfort symptoms of the reproductive tract, while women recruited in our study had more understanding of HPV and wanted to put HPV screening into the routine practice. HPV prevalence in different regions may be attributed to the geographical regions, economic level, method of sampling, and screening technology. The sample size is another possible cause for this variation from other studies; while our study included 150639 women. Another reason for the differences may be the survey period; which, in our study was 2014–2018, and that in Chengdu, Henan, Zhejiang, Xinjiang, Harbin, Fujian was 2016–2017 [14], 2012–2013 [15], 2006–2008 [16], 2008–2018 [17], May to December of 2011 [18], 2009–2015 [8], respectively. Further research would enable clarification of the extent to which these results are affected by demographic differences of the study samples and the methods for virus testing.
The HPV infection rate in the Health Management Center was 14.4% which was lower than that in Guangdong (17.25%)[20]. The prevalence of HR-HPV infection was 11.7%, which was nearly similar to that in Sichuan (12.6%)[21]. The cause of this may be the close geographical location of Chongqing and Sichuan and the similar laboratory detection methods.
As observed in this study, the most common genotype for HR-HPV detected in this study was HPV 52, followed by HPV16, 58, 53, 56, and 18. The most common genotype for LR-HPV was HPV 61, followed by 81, 43, 44, 6, and 11. The results were different from those in Chengdu which is adjacent to Chongqing. In the northern part of Chengdu, the primary genotypes were found to be HPV 52, 58, 16, 53, and 39 [14]. Our results were also different from those of the previous report from Chongqing, which showed that the top five genotypes were HPV 16, 52, 58, 18, and 33 [13]. We hypothesize that this variation maybe because of the study period and participants. The most prevalent types of HR-HPV infection in Health Management Center were HPV52, 58, 53, 16 in this order, different from the types in Sichuan (HPV52, 53, 58, 16 in this order) [21]. Some studies have reported that HPV 52 and 58 were more dominant genotypes and relate to cervical cancer occurrence in the Asian population [22–24]. HPV16, irrespective of age, played a primary role in ≥ CIN3development, while HPV18 also significantly contributed to adenocarcinomain situ (AIS) and cancer [25]. In this study, we found that the main prevalent genotype in Chongqing province was HPV 52, followed by HPV 16. It has confirmed that the main HPV genotypes were HPV16, 18, 58, 52, and 33 in cervical cancer [26]. HPV 16, 18, and 56 were significantly associated to worsen histology [27]. Therefore, the identification of HR HPV in primary screening is imperative for all women.
While the types of the HPV vaccine are specific, current vaccines cannot completely protect against non-vaccine HPV genotypes. According to our study, two valent HPV (targets HPV 16, and 18) and four valent HPV (targets HPV 6, 11, 16, and 18) cover only 22.5% and 27.3% of infections, respectively. On assessing the nine-valent HPV (targets HPV 6, 11, 16, 18, 31, 33, 45, 52, and 58), an increase was observed in the ability to prevent HPV to 64.3% in Chongqing women.
While the earlier studies indicated the highest HPV infection prevalence among 41–45 years old women [28, 29], in this survey, the age-related distribution of HPV infection in total HPV, double HPV, triple HPV, and quadruple, or more all showed bimodal age distribution. The first peak at less than 24 years of age may be because of sexual activity [30] and underdeveloped immunity to HPV [31]. The second peak at ≥ 55 years of age may be because of HPV persistence and latent virus reactivation due to the dysregulation (physiologic and immunologic) in the menopausal transition period [32] and may have an increased risk of cervical cancer development. The lowest rate of HPV infection rate was observed in the 25–34 age group, possibly because of their developed immunity against HPV, for better prevention and clearing HPV infections.
Some studies reported a significant increase in multiple HPV infections in the duration of infection and their frequent detection in cervical cancer of different grades [33]. In this investigation, the prevalence of multiple HPV accounted for 22.5% of the total positive cases. In terms of age-specificity, multiple HPV infection prevalence exhibited a “U-shaped” curve and these represented the younger women and older women. The lowest prevalence was in the 35–44 age group. This was similar to that observed in Zhengzhou [34]. Thus, the multiple infections and their effect in this region warrant further investigation. Our finding could also be significant in the development of HPV vaccines, although its development and effective application may be more complex because of multiple infections.
This study had a few limitations. This study included only those women who attended the First Affiliated Hospital, Chongqing Medical University and tested for HPV, indicating that these outcomes may not be representative of all women in Chongqing. Further, we only analyzed the HPV infection prevalence and distribution of its genotypes, but not the relationship between HPV, cytology, and histology, which will be further explored in the next study. Third, the recording of all participants and the information about receiving the HPV vaccine in Chongqing were not carried out. Therefore, potential HPV infections could not be evaluated after vaccination. Finally, the HPV results of only the first examination were collected, and the results of the next HPV test were not included. Hence, we cannot analyze the difference of HPV subtypes distribution before and after therapy. In the future, there is a need for more in-depth research to evaluate HPV infection.