Norway’s first comprehensive national surveillance shows HPV16 and HPV18 remain dominant in cervical disease, but early signs of vaccine-driven pattern changes emerge in younger women, prompting a need for ongoing monitoring of disease evolution.
Norway’s first national surveillance data on human papillomavirus types in cervical disease suggest that the main cancer-causing strains are still HPV16 and HPV18, but that vaccination is already changing the pattern in younger women. In the study published in the International Journal of Cancer, researchers linked genotype results from the country’s mandatory cervical surveillance system with immunisation records to compare unvaccinated women with those eligible for Norway’s vaccine programmes.
The analysis covered cases of cervical intraepithelial neoplasia grade 2 or 3, adenocarcinoma in situ and invasive cervical cancer. In the unvaccinated baseline group, HPV16 remained the most common type across all three conditions, followed by HPV18 in more advanced disease, while HPV31, HPV33, HPV45, HPV52 and HPV58 also made meaningful contributions. For invasive cancer, the researchers found that roughly three-quarters of cases were attributable to HPV16 or HPV18, with HPV45, HPV33 and HPV31 next in line. Nearly all adenocarcinoma in situ cases were linked to HPV18, HPV16 or HPV45.
The study also points to an early vaccine effect. Among women eligible for routine childhood immunisation, HPV16 almost disappeared from cervical precancer in those vaccinated before age 15, and HPV18 was not seen in that group. A smaller but still clear reduction in HPV16 was also seen among women vaccinated later in adolescence. In the catch-up cohort, which received vaccine after the main childhood programme began, the overall pattern was broadly similar in vaccinated and unvaccinated women, although HPV16 attribution was lower in vaccinated cases of high-grade precancer. The effect was much less obvious for adenocarcinoma in situ and invasive cancer, which the authors said is unsurprising because many of those women were infected before vaccination or were too old to have benefited fully.
The findings matter because Norway has built a rare national system for monitoring HPV types in cervical lesions, combining pathology review with sequential genotyping of 37 HPV strains. That allowed the researchers to compare crude prevalence with proportional attribution, a method that tries to assign each lesion to the most likely causal type when more than one HPV strain is present. The two approaches produced very similar results, suggesting the headline conclusions are robust. The study also found that the age burden of disease differed by lesion type: cervical precancer peaked in women aged 25 to 34, while invasive cancer was most common in women aged 35 to 44.
Researchers said the data provide a baseline for measuring the long-term effect of Norway’s vaccination programme, which first offered free HPV vaccine to girls born in 1997 or later and later expanded to boys. They also noted that the rise of non-vaccine types in vaccinated women does not mean these strains are becoming more dangerous; rather, when HPV16 and HPV18 fall, other types make up a larger share of a shrinking total. The practical implication, the authors said, is that screening and surveillance will need to keep tracking how the disease mix changes as vaccinated generations reach the age when cervical abnormalities are usually detected.
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