title: Sexual behavior, human papillomavirus type 16 (HPV 16) infection, and HPV 16 seropositivity.
abstract: BACKGROUND
  Sexual behaviors have been linked to seropositivity for human papillomavirus (HPV) but not with the magnitude of the seroreactivity.
  
  
  OBJECTIVE
  The objective of this analysis was to examine the association of sexual behavior, cervical HPV 16 DNA positivity at enrollment (past) and at diagnosis (current), and other potential determinants with the likelihood and magnitude of HPV 16 seropositivity at diagnosis.
  
  
  METHODS
  With use of stored specimens from an incidence case-control study at Kaiser Permanente (Portland, OR), women were tested for seroreactivity to HPV 16 by enzyme-linked immunosorbent assay with virus-like particles at diagnosis and were tested for past and concurrent cervical HPV 16 DNA positivity with MY09/MY11 L1 consensus primer PCR. Questionnaire data were used to ascertain past sexual behavior.
  
  
  RESULTS
  Increased lifetime number of sex partners (P(Trend) < 0.001), past HPV 16 DNA positivity (odds ratio = 6.9; 95% confidence interval = 1.5-31), and a current cytologic diagnosis (P(Trend) < 0.03) were independently associated with HPV 16 seropositivity. Among the seropositive, only lifetime number of sex partners (P(Trend) < 0.001) and past HPV 16 DNA positivity (P = 0.003) were independently associated with mean signal strength (optical density) in an age-adjusted analysis. Women negative for past and concurrent HPV 16 DNA had a significant trend of increasing optical densities associated with greater numbers of lifetime partners (P(Trend) < 0.001). Conversely, the mean signal strength for those women who were ever HPV 16 DNA-positive during the study did not depend on lifetime numbers of sex partners (P(Trend) = 0.36).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland 20892, USA. pc95p@nih.gov
authors.forename: Philip E
authors.initials: PE
authors.lastname: Castle
authors.forename: Tammy
authors.initials: T
authors.lastname: Shields
authors.forename: Reinhard
authors.initials: R
authors.lastname: Kirnbauer
authors.forename: M Michele
authors.initials: MM
authors.lastname: Manos
authors.forename: Robert D
authors.initials: RD
authors.lastname: Burk
authors.forename: Andrew G
authors.initials: AG
authors.lastname: Glass
authors.forename: Daivid R
authors.initials: DR
authors.lastname: Scott
authors.forename: Mark E
authors.initials: ME
authors.lastname: Sherman
authors.forename: Mark
authors.initials: M
authors.lastname: Schiffman
mesh_terms: D000328:Adult; D000914:Antibodies, Viral / Q000097:blood*; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D008875:Middle Aged; D015999:Multivariate Analysis; D016017:Odds Ratio; D027383:Papillomaviridae / Q000276:immunology / Q000302:isolation & purification*; D030361:Papillomavirus Infections / Q000097:blood / Q000175:diagnosis*; D012725:Sexual Behavior; D012747:Sexual Partners; D011795:Surveys and Questionnaires; D014412:Tumor Virus Infections / Q000097:blood / Q000175:diagnosis*
chemical_list: D000914:Antibodies, Viral