Behavioral and sociodemographic risk factors for serological and DNA evidence of HPV6, 11, 16, 18 infections

Dorothy J. Wiley, Emmanuel V. Masongsong, Shuang Lu, Sings Heather L., Benissa Salem, Anna R. Giuliano, Kevin A. Ault, Richard M. Haupt, Darron Brown

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Introduction: Risk for HPV6/11/16/18 infections in young sexually active, behaviorally low-risk females is not well described and may inform public policy. Methods: To assess exposure risk for HPV/6/11/16/18 among 16-23 year old low-risk females, data for 2409 female clinical trial participants were evaluated. Baseline visit self-reported sexual, behavioral and demographic characteristics; and results from HPV genotyping and serology, and other clinical laboratory assays were analyzed. All subjects reported <5 lifetime male sexual partners and no prior abnormal cytology at baseline. Results: While 98% (2211/2255) were naïve to HPV16 or 18 and 99.6% (2246/2255) were naïve for 1-3 index HPVs, 27% (616/2255) showed antibody, DNA or both for ≥1 index HPV. While 18% (409/2255) tested HPV16- or -18-antibody- or -DNA-positive, only 2% (44/2255) tested positive for both types. Against this high background, other sexually transmitted infections (STIs) were uncommonly detected, suggesting low sexual risk-taking behavior. The adjusted analyses showed race, age, alcohol consumption, current Chlamydia trachomatis (chlamydia) and Trichamonas vaginalis (trichomoniasis), bacterial vaginosis (BV), number of lifetime male sex partners predicted positive index-HPV antibody test results. However, only the number of male sex partners predicted positivity for HPV6/11- and 16/18-DNA, and chlamydia infection predicted positivity for HPV6/11-DNA alone. Conclusions: Taken together, type-specific HPV-DNA and -antibody evidence of HPV6/11/16/18 infections among behaviorally low-risk 16-23 year old females is high. Since almost all participants would have benefited by either currently available bivalent or quadrivalent vaccine strategies, delaying vaccination beyond menarche may be a missed opportunity to fully protect young females against HPV6/11/16/18 infections and related dysplasias. Early diagnosis and treatment of chlamydia and trichomonas may be important in HPV pathogenesis.

Original languageEnglish
JournalCancer Epidemiology
Volume36
Issue number3
DOIs
StatePublished - Jun 2012

Fingerprint

DNA
Infection
Chlamydia
Antibodies
Trichomonas
Human papillomavirus 11
Human papillomavirus 6
Bacterial Vaginosis
Chlamydia Infections
Menarche
Sexual Partners
Chlamydia trachomatis
Serology
Public Policy
Sexually Transmitted Diseases
Risk-Taking
Alcohol Drinking
Cell Biology
Early Diagnosis
Vaccination

Keywords

  • Bacterial vaginosis and HPV
  • Cervicovaginal infections
  • Chlamydia and HPV
  • HPV behavioral risk factors
  • HPV-DNA detection
  • HPV-infection
  • HPV-serology
  • Trichomonas and HPV

ASJC Scopus subject areas

  • Cancer Research
  • Oncology
  • Epidemiology

Cite this

Behavioral and sociodemographic risk factors for serological and DNA evidence of HPV6, 11, 16, 18 infections. / Wiley, Dorothy J.; Masongsong, Emmanuel V.; Lu, Shuang; Heather L., Sings; Salem, Benissa; Giuliano, Anna R.; Ault, Kevin A.; Haupt, Richard M.; Brown, Darron.

In: Cancer Epidemiology, Vol. 36, No. 3, 06.2012.

Research output: Contribution to journalArticle

Wiley, DJ, Masongsong, EV, Lu, S, Heather L., S, Salem, B, Giuliano, AR, Ault, KA, Haupt, RM & Brown, D 2012, 'Behavioral and sociodemographic risk factors for serological and DNA evidence of HPV6, 11, 16, 18 infections', Cancer Epidemiology, vol. 36, no. 3. https://doi.org/10.1016/j.canep.2011.12.007
Wiley, Dorothy J. ; Masongsong, Emmanuel V. ; Lu, Shuang ; Heather L., Sings ; Salem, Benissa ; Giuliano, Anna R. ; Ault, Kevin A. ; Haupt, Richard M. ; Brown, Darron. / Behavioral and sociodemographic risk factors for serological and DNA evidence of HPV6, 11, 16, 18 infections. In: Cancer Epidemiology. 2012 ; Vol. 36, No. 3.
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AU - Wiley, Dorothy J.

AU - Masongsong, Emmanuel V.

AU - Lu, Shuang

AU - Heather L., Sings

AU - Salem, Benissa

AU - Giuliano, Anna R.

AU - Ault, Kevin A.

AU - Haupt, Richard M.

AU - Brown, Darron

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N2 - Introduction: Risk for HPV6/11/16/18 infections in young sexually active, behaviorally low-risk females is not well described and may inform public policy. Methods: To assess exposure risk for HPV/6/11/16/18 among 16-23 year old low-risk females, data for 2409 female clinical trial participants were evaluated. Baseline visit self-reported sexual, behavioral and demographic characteristics; and results from HPV genotyping and serology, and other clinical laboratory assays were analyzed. All subjects reported <5 lifetime male sexual partners and no prior abnormal cytology at baseline. Results: While 98% (2211/2255) were naïve to HPV16 or 18 and 99.6% (2246/2255) were naïve for 1-3 index HPVs, 27% (616/2255) showed antibody, DNA or both for ≥1 index HPV. While 18% (409/2255) tested HPV16- or -18-antibody- or -DNA-positive, only 2% (44/2255) tested positive for both types. Against this high background, other sexually transmitted infections (STIs) were uncommonly detected, suggesting low sexual risk-taking behavior. The adjusted analyses showed race, age, alcohol consumption, current Chlamydia trachomatis (chlamydia) and Trichamonas vaginalis (trichomoniasis), bacterial vaginosis (BV), number of lifetime male sex partners predicted positive index-HPV antibody test results. However, only the number of male sex partners predicted positivity for HPV6/11- and 16/18-DNA, and chlamydia infection predicted positivity for HPV6/11-DNA alone. Conclusions: Taken together, type-specific HPV-DNA and -antibody evidence of HPV6/11/16/18 infections among behaviorally low-risk 16-23 year old females is high. Since almost all participants would have benefited by either currently available bivalent or quadrivalent vaccine strategies, delaying vaccination beyond menarche may be a missed opportunity to fully protect young females against HPV6/11/16/18 infections and related dysplasias. Early diagnosis and treatment of chlamydia and trichomonas may be important in HPV pathogenesis.

AB - Introduction: Risk for HPV6/11/16/18 infections in young sexually active, behaviorally low-risk females is not well described and may inform public policy. Methods: To assess exposure risk for HPV/6/11/16/18 among 16-23 year old low-risk females, data for 2409 female clinical trial participants were evaluated. Baseline visit self-reported sexual, behavioral and demographic characteristics; and results from HPV genotyping and serology, and other clinical laboratory assays were analyzed. All subjects reported <5 lifetime male sexual partners and no prior abnormal cytology at baseline. Results: While 98% (2211/2255) were naïve to HPV16 or 18 and 99.6% (2246/2255) were naïve for 1-3 index HPVs, 27% (616/2255) showed antibody, DNA or both for ≥1 index HPV. While 18% (409/2255) tested HPV16- or -18-antibody- or -DNA-positive, only 2% (44/2255) tested positive for both types. Against this high background, other sexually transmitted infections (STIs) were uncommonly detected, suggesting low sexual risk-taking behavior. The adjusted analyses showed race, age, alcohol consumption, current Chlamydia trachomatis (chlamydia) and Trichamonas vaginalis (trichomoniasis), bacterial vaginosis (BV), number of lifetime male sex partners predicted positive index-HPV antibody test results. However, only the number of male sex partners predicted positivity for HPV6/11- and 16/18-DNA, and chlamydia infection predicted positivity for HPV6/11-DNA alone. Conclusions: Taken together, type-specific HPV-DNA and -antibody evidence of HPV6/11/16/18 infections among behaviorally low-risk 16-23 year old females is high. Since almost all participants would have benefited by either currently available bivalent or quadrivalent vaccine strategies, delaying vaccination beyond menarche may be a missed opportunity to fully protect young females against HPV6/11/16/18 infections and related dysplasias. Early diagnosis and treatment of chlamydia and trichomonas may be important in HPV pathogenesis.

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KW - Cervicovaginal infections

KW - Chlamydia and HPV

KW - HPV behavioral risk factors

KW - HPV-DNA detection

KW - HPV-infection

KW - HPV-serology

KW - Trichomonas and HPV

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