We observed an overall hrHPV prevalence in line with rates previously reported in screening populations from China or Asian [11, 12]. Notably, there was a relatively high prevalence of hrHPV among women under 30 years old, with a slight decrease observed in older age groups. However, unlike the typical U-shaped curve, the age-related variation of HPV prevalence in this cohort was relatively flat. We think it may be related to the conservative sexual attitudes of young women in this area.

Recently, a viewpoint published on Lancet Public Health suggested that risk-based strategies appear to be the most effective way for screening services to recover following disruptions related to the COVID-19 pandemic and the implementation of an age-based risk stratification should be universally feasible [13]. However, the correlation between the risk of cervical precancer following HPV infection and age has not been consistently supported by several previous studies [3,4,5,6,7,8]. It is reported that the 10-year risk of CIN3 + among women with positive HC2 test and a concurrent negative cytology in younger group aged 22–32 was lower than in older group aged 40–50 (13.6% vs. 21.2%) [3]. A cohort study from Taiwan revealed that the cumulative CIN3 + risks following persistent HPV infections increased with age (5.5%, 14.4%, and 18.1% for women aged 30–44 years, 45–54 years, and ≥ 55 years, respectively) [4]. Inconsistently, a subanalysis of the ATHENA data revealed that The CIN 2 + risk was lower in HPV16-positive women aged 40 years or older compared to women under 40 years (16% versus 35%) [5]. Similarly, a large cohort study from Kaiser Permanente Northern California (KPNC) showed that the 5-year CIN 3 + risk did not increase with age but decreased slightly for either women with enrollment HPV infections or newly detected HPV infections [6]. Additionally, the 3-year cumulative risk of developing ≥ HSIL in a cohort of 9434 women varied significantly with age, with the highest risk noted among women aged < 40 years [7]. Lately, a real-world data from Norway indicated that the overall CIN3 + risk was higher for younger women aged 34–43 compared to older women aged 44–69 (30.6% vs. 18.1%) [8].

In this cohort, the 3-year cumulative risks of CIN2 + and CIN3 + in women infected with HPV didn’t show a significant age-related increase but rather a certain decline. If stratified by median age (48 years) of this cohort, the cumulative risks of high-grade CIN in women positive for hrHPV at baseline were significantly higher in younger age group than in older age group. Our result supports that younger HPV-positive women have a higher risk of developing cervical precancer, which is consistent with several reports [5,6,7,8] published in recent years but contrary to the earlier studies [3, 4]. One possible explanation is that women who are genetically susceptible to cervical cancer have developed the precancerous diseases earlier and have been previously identified and treated at their younger ages. While women with low susceptibility to cervical cancer are less likely to develop the disease even years later. It is noteworthy that the incidence of cervical cancer in young women (15–49 years) is increasing globally from 1990 to 2019, especially in areas with high sociodemographic index [14]. Although most cervical cancer burden can be eliminated by HPV-based vaccination and screening, it is urgent to control the younger trend. Noticing the risk of cervical lesions in younger women infected with HPV maybe helpful to control the younger trend of cervical cancer.

There are still some deficiencies in this study. Firstly, the retrospective cohort was consisted of 2 separate screening populations, with several variables that were difficult to control, such as colposcopy referral protocol and screening history. Secondly, due to the ethical considerations, almost all of the women with negative co-testing results were not referred to colposcopy and were all regarded as CIN1 or less. These might result in a lower disease prevalence in this cohort and the risk of CIN2 + would be underestimated. Choosing CIN2 + as the study endpoint is another limitation. Because CIN2 has appreciable regression rates and the pathological diagnosis of CIN2 is less reproducible. Moreover, the short period of follow-up, as well as the limited number of cases in the youngest and oldest age groups, which may cause some deviation in the research results. Large-scale prospective studies with extended HPV genotyping are needed to validate the findings of the current study.

In summary, our study highlights the potential value of age-specific risk stratification in cervical cancer screening.