Human papillomavirus (HPV) infection in older women is commonly due to reactivation of latent disease rather than new infection, research indicates.
The study, published in The Journal of Infectious Diseases, showed that the age-specific prevalence of HPV rose with the number of sexual partners, a finding of particular relevance to women who became sexually active during the sexual revolution of the 1960s and 1970s, say the researchers.
"Our historical experience with HPV and cervical neoplasia in postmenopausal women may not be very predictive of the experience of the baby boomer generation of women who are now entering the menopausal transition at a higher risk than their mothers," remarked study co-author Patti Gravitt (Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA) in an accompanying press statement.
Gravitt and colleagues explored age-related fluctuations in HPV infection in the USA, where the prevalence peaks among younger women around the age of sexual debut. In other geographic regions there is a second attenuated peak around the age of menopause but this bimodal distribution is not seen in the US.
"Explanations for this variability include differences in relative prevalence of new partnerships at older ages, risk of HPV reactivation at older ages, and cohort effects," writes the team.
They enrolled 843 women aged 35-60 years and tested them for HPV DNA. The women's mean age was 46.6 years, 74.3% were White, and 19.0% were Black.
The prevalence of HPV - whether all types combined or just high-risk strains - decreased with age and increased with the number of lifetime sexual partners, with a threshold observed between four and five such partners. HPV prevalence was also higher among women with a recent new sexual partner.
Interestingly, the prevalence of HPV declined with increasing age among women with fewer than five lifetime sex partners. However, among women reporting five or more lifetime partners, the prevalence of any HPV and high-risk HPV declined between ages 35-40 years, increased again during ages 40-54 years, and then decreased at ages 55-60 years.
The interaction between age and lifetime number of sex partners was modest for any HPV and statistically significant for high-risk HPV, after adjustment for recent sexual behavior, marital status, history of colposcopy, and current cytologic abnormality.
This finding is consistent with an age-associated increased risk of HPV reactivation, say the authors. The older women in this study, who experienced sexual debut at the beginning of the US sexual revolution of the 1960s and 1970s, had a lower lifetime risk for HPV infection as demonstrated by a lower self-reported lifetime number of sex partners, they note.
Gravitt and co-authors conclude: "We propose that the cohort effect of the sexual revolution in the USA is masking an increase in HPV prevalence at older ages, which may be secondary to reactivation of 'latent' infection. Further follow-up of the HPV in perimenopause cohort and national surveillance data will be required to confirm this hypothesis."
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