In this study, we examined the epidemiology of HPV and risk factors associated with high-risk and vaccine-type HPV infection in a racially and ethnically diverse, predominantly low-income population of sexually experienced young women eligible for “catch-up” HPV vaccination. The cross-sectional prevalence of HPV in this sample was high at 68%: this likely underestimates the cumulative lifetime prevalence of HPV as most infections do not persist. Previous studies of predominantly low-income adolescents have demonstrated similarly high prevalence rates.19, 20
In contrast, the prevalence of HPV in study samples that are more representative of the U.S. population is considerably lower,21
supporting the growing evidence that poverty is a strong predictor of HPV infection.14
The high rates of HPV infection in our study sample, combined with evidence that HPV is often acquired soon after sexual initiation,22
suggest that vaccinating young women prior to sexual initiation must be a priority to maximize both the individual and population-level health benefits of vaccination.
Although almost 70% of participants were positive for HPV, fewer than 20% were positive for HPV-16 or HPV-18, < 5% were positive for both HPV-16 and HPV-18, and none was infected with all four vaccine types. HPV vaccines do not have clinical benefit in women who are infected with vaccine-type HPV at the time of vaccination; however, women who are uninfected with some of those types should derive partial benefit from vaccination.23
Thus, even in this sample of women, who had a very high overall HPV prevalence rate, the majority would be expected to benefit at least partially from vaccination. The findings do not address the question of whether vaccination of sexually active women will be cost-effective or have population-level benefit, but they provide evidence that individual women are likely to benefit.
In addition to HPV-16 and HPV-18, one of the most commonly identified HPV types was HPV-52. Global epidemiologic studies suggest that HPV-52 prevalence varies across regions but is particularly common in Africa and Asia.24-26
Although HPV-52 has substantially lower potential to cause cervical neoplasia in comparison to HPV-16 and HPV-18,27, 28
these high prevalence rates are concerning as HPV-52 is not targeted by the two licensed vaccines. To our knowledge, previous studies have not examined risk factors for HPV-52. In this study, risk factors were similar for HPV-52 as for other high-risk types, with the exception of anal sex, which was associated only with HPV-52. Additional information is needed regarding the epidemiology of HPV-52, its role in carcinogenesis, and what clinical significance it will have in the vaccination era.
Identification of factors associated with high-risk and vaccine-type HPV infection may help to inform decisions about vaccine delivery and the design of interventions to prevent infection. Our finding that Black race and number of sexual partners were associated with high-risk HPV is consistent with previous studies.14, 19, 29, 30
However, a previous analysis suggests that higher rates of HPV infection in Black compared to White women are explained in large measure by racial differences in marital status and income. In that study, Black women were more likely than White women to be unmarried and poor, and those socioeconomic factors explained racial differences in HPV infection.14
Racial differences may also be driven by unmeasured disparities in social and economic assets related to income, such as wealth, community resources, and access to health services and education. The findings suggest that minority and low-income women must have enhanced access not only to HPV vaccines, but also to education and other preventive health services to prevent cervical cancer, including Pap screening. Culturally sensitive educational interventions about HPV vaccines are especially important for minority women, as mistrust of medical professionals and the government may underlie concerns about new vaccines among Black women.31-34
In this study sample, measures of recent sexual activity were not independently associated with high-risk HPV infection, whereas lifetime number of sexual partners was associated with infection. Our findings are similar to that of a study of sexually active urban adolescents.19
Number of lifetime partners may be a more reliable and stable measure of exposure to HPV and other STI in adolescent and young adult women because number of recent partners may not be a reliable marker of sexual history; for example, among those with few recent partners, there may be substantial variation in lifetime number of partners. In contrast to the findings related to high-risk HPV infection, no variables were independently associated with vaccine-type HPV infection, supporting current recommendations for universal vaccination.
This study has several limitations. Because participants were predominantly minority and low-income, and because only sexually experienced women were included, the results are not generalizable to all young women eligible for catch-up HPV vaccination. Sexual and gynecologic history was self-reported, possibly limiting validity. We did not include income measures, limiting our ability to explore associations between poverty, race, and HPV infection. The HPV assay used in this study included several high-risk types that are not included in the HPV tests that are commercially available and commonly used in clinical practice; therefore, HPV prevalence in this study may be higher than if a routine clinical test were used. Despite these limitations, this study provides novel data about the prevalence and risk factors associated with type-specific HPV infection in a diverse sample of sexually experienced women, shortly after the quadrivalent HPV vaccine was licensed in the U.S. Our findings provide support for universal vaccination of sexually experienced 13-26 year-old young women in the U.S.