HPV is an important international carcinogenic infection. The 12 high-risk types are reported to be the second most common infectious cause of cancer worldwide after Helicobacter pylori.17
Most HPV infections occur within the first two years of onset of sexual activity, with more than 40 percent becoming infected during this period. The first sexual relationship carries a substantial risk.18
Data from the NZ Youth 2012 survey19, 20 suggests that approximately 8 percent of New Zealand adolescents may have had sexual intercourse before the age of 13 years. This increases to 24 percent by the age of 15 years and 46 percent by age 17 years.
Compared to 2001, students were more likely to delay sexual debut in 2012 but less likely to use condoms and contraception consistently.21 Māori (OR 0.7; 95% CIs: 0.6–0.8) and Pacific (OR 0.5; 95% CIs: 0.4–0.7) students used condoms less frequently than NZ European students; those from areas with high levels of deprivation (OR 0.7; 95% CIs: 0.5–0.9) also used condoms less frequently than students from areas of low deprivation.21
In approximately 15 percent of women with persistent HPV16 infection, CIN3 develops about 7 to 15 years after acquiring the infection. The risk of cancer in women with persistent infection due to HPV18 is approximately 10 percent, while the risk due to persistent infection with all other oncogenic serotypes is less than 5 percent.
The incidence of cervical cancer in developed nations is approximately 10–15 per 100,000 women aged 20–70 years, with an annual mortality of approximately 5–8 per 100,000.
The prevalence of HPV infection and distribution of HPV types among New Zealand women with histologically-confirmed CIN 2/3 22, 23 or invasive cervical cancer24 is broadly consistent with that seen internationally. In women with histologically-confirmed CIN 2/3, 97 percent (95% CI: 94–98) were HPV-positive and the prevalence of any high-risk HPV was 96 percent (95% CI: 91–99).22 In women with histologically-confirmed invasive cervical cancer, 88.5 percent (95% CI: 83.7–92.4) were HPV-positive, and the prevalence of any high-risk HPV was 87.2 percent (95% CI: 82.2–91.3).24 For both CIN2/3 and invasive cervical cancer, the overall distribution of HPV types was similar in Māori and non-Māori women, with HPV16 being the most commonly detected HPV type in both groups.22, 24
In 2015 there were 138 new cervical cancer registrations, down from 143 in 2014 (provisional data)25. The age-standardised registration rate was 5.3 per 100,000 population, similar to the 2014 rate (5.5 per 100,000). The registration rate for Māori women was 9.7 per 100,000, 2.1 times greater than for non-Māori women (4.7 per 100,000).
The most recent cervical cancer mortality data is from 2013, when there were 54 deaths (1.7 deaths per 100,000 population).26 The mortality rate for Māori women was 4.0 per 100,000, 2.9 times greater than for non-Māori women (1.4 per 100,000).
HPV types 16, 18, 31, 33, 45, 52 and 58 are linked to other cancers in women and men, including vulval, vaginal, penile, anal and oropharyngeal cancers (see Table 9.1).
In 2013, there were 56 vulval, 23 vaginal, 19 penile, 70 anal (38 women, 32 men) and 16 oropharyngeal (5 women, 11 men) new cancer registrations.26
Genital warts, which are most commonly due to infection with HPV6 or HPV11, have a prevalence of approximately 1 percent of adults in the US.27, 28 In Scandinavian countries the reported rates are as high as 10 percent.29
Sexually transmitted infections (STIs) are not notifiable in New Zealand. The Institute of Environmental Science and Research (ESR) cautions that the number of cases of STIs reported through the clinic-based surveillance system likely underestimates the true burden of disease in New Zealand because a substantial percentage of STIs are diagnosed by other health care providers.
From 200930 to 201531 genital warts clinical case counts reported by sexual health clinics (SHCs) decreased by 54.3 percent (from 3290 to 1504 cases) and case counts reported by family planning clinics (FPCs) decreased by 65.6 percent (from 546 to 188 cases). In SHCs there was a decrease in diagnoses in all ethnic groups, except ‘Other’ ethnicity. In FPCs, the number of diagnoses decreased in every ethnic group.
In SHCs, the decrease was most notable in the 15–19 years and 20–24 years age groups, and a moderate decrease in the 25–29 years age group, in both sexes (Figure 9.1). The decrease seen in older age groups suggests that immunisation is also providing some herd immunity to unvaccinated individuals. A decline in the number of prescriptions for treating genital warts (imiquimod and podophyllum resin-based products) supports this evidence for a herd immunity effect.32 The largest decline was seen in women aged under 20 years.
Source: Institute of Environmental Science and Research