No abstract

Human papillomavirus (HPV) seroprevalence and determinants of seropositivity were assessed in a 10 049-woman population-based cohort in Guanacaste, Costa Rica. Serologic responses based on VLP-based ELISA were obtained from the plasma collected at study enrollment in 1993/1994 for HPV-16 (n ¼ 9949), HPV-18 (n ¼ 9928), HPV-31 (n ¼ 9932), and HPV-45 (n ¼ 3019). Seropositivity was defined as five standard deviations above the mean optical density obtained for studied virgins (n ¼ 573). 15, 16, and 11%, respectively. Of women DNA-positive for , seropositivity was 45, 34, 51, and 28%, respectively. Peak HPV seroprevalence occurred a decade after DNA prevalence; lifetime number of sexual partners was the key determinant of seropositivity independent of DNA status and age. DNA-and sero-positive women showed the highest risk for concurrent CIN3/cancer, followed by DNA-positive, sero-negative women. British Journal of Cancer (2003) (Ho et al, 1995). The prevalence of HPV DNA therefore underestimates the cumulative incidence of infection in a population, particularly where the majority of women will not develop persistent infection or cervical neoplasia. Measurement of serum antibody to HPV capsids (or virus-like particles (VLPs)) has been demonstrated as a useful although imperfect marker of past and cumulative HPV exposure, thus complementing the assessment of HPV DNA (Kirnbauer et al, 1994;Wideroff et al, 1995Wideroff et al, , 1999Carter et al, 1996;Sasagawa et al, 1998;Touze et al, 2001).As part of a large population-based study of the natural history of HPV infection and cervical neoplasia in Guanacaste, Costa Rica, we report here the population-based seroprevalence in Guanacaste women of four oncogenic HPV types found in the majority of cervical cancers worldwide Munoz et al, 2003). The data presented document the baseline burden of HPV exposure in Guanacaste, Costa Rica. As a major objective, we determined the association of risk for concurrent diagnosis of CIN3/cancer with HPV assessed jointly by serology and PCR-based DNA testing. As only about half of all HPV-DNA-positive women are seropositive using available VLP assays (Kirnbauer et al, 1994;Le Cann et al, 1995), we also investigated determinants of seropositivity in our population. METHODS Study populationThis study was conducted in an on-going population-based cohort study of 10 049 women in Guanacaste, Costa Rica (Herrero et al, 1997;Hildesheim et al, 2001) who were enrolled in 1993 -1994 with the approval of the National Cancer Institute (NCI) and local institutional review boards; all participants provided written informed consent. Briefly, the cohort was a representative sample of the adult population based on selection by cluster sampling, with oversampling for cancer. Participation among eligible women exceeded 90%, and participants completed a risk factor questionnaire that addressed demographic, behavioural, and sexual practices. Women were screened using three cytologic and one visual test at enrollment; colposcopy referral with biopsy was perform...

Previously, we have demonstrated that sperm from the Pacific herring, Clupea palLasi, remain immotile upon spawning into the surrounding medium and initiate motility only upon contact with the micropyle area ofthe chorion (Yanagimachi et al., '92, Dev. Growth Differ., 34:447-461).In the present study we have purified a chorion-bound sperm motility initiating factor (SMIF) and have found it to be a 105 kDa glycosylated polypeptide. The isolated factor was highly bioactive, stimulating prolonged motility in >90% of the cells in vitro. The 105 kDa glycoprotein showed affinity for Con A on western blots. Furthermore, in intact eggs, Con A was localized to only the micropyle area, indicating that SMIF is restricted to this region of the chorion. o 1993 Wiley-Liss, Inc.

In this large study, we have confirmed some results from smaller studies and identified some new relationships that need to be confirmed elsewhere.

HPV 16 seropositivity is a surrogate for past HPV 16 infection. Circulating levels of antibodies to HPV 16 may reflect recent HPV 16 infection or the frequency of past HPV 16 infection.