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Original research
Human papillomavirus and abnormal cervical lesions among HIV-infected women in HIV-discordant couples from Kenya
  1. Brandon L Guthrie1,
  2. Anne F Rositch2,
  3. Joy Alison Cooper3,
  4. Carey Farquhar4,
  5. Rose Bosire5,
  6. Robert Choi6,
  7. James Kiarie7,
  8. Jennifer S Smith8
  1. 1 Departments of Global Health and Epidemiology, University of Washington School of Public Health, Seattle, Washington, USA
  2. 2 Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, USA
  3. 3 Department of Obstetrics and Gynecology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA
  4. 4 Departments of Global Health, Epidemiology, and Medicine, University of Washington, Seattle, Washington, USA
  5. 5 Center for Public Health Research, Kenya Medical Research Institute, Nairobi, Kenya
  6. 6 Department of Global Health, University of Washington School of Public Health, Seattle, Washington, USA
  7. 7 Department of Reproductive Health and Research, World Health Organization (WHO), Geneva, Switzerland
  8. 8 Department of Epidemiology, Lineberger Comprehensive Cancer Center, University of North Carolina Gillings School of Global Public Health, Chapel Hill, North Carolina, USA
  1. Correspondence to Dr Jennifer S Smith, Department of Epidemiology, University of North Carolina Gillings School of Global Public Health, Chapel Hill, NC 27599, USA; jsssmith{at}


Objective HIV infection increases the risk of high-grade cervical neoplasia and invasive cervical carcinoma. The study addresses the limited data describing human papillomavirus (HPV) infection and cervical neoplasia among HIV-infected women in HIV-discordant relationships in sub-Saharan Africa, which is needed to inform screening strategies.

Methods A cross-sectional study of HIV-infected women with HIV-uninfected partners was conducted to determine the distribution of type-specific HPV infection and cervical cytology. This study was nested in a prospective cohort recruited between September 2007 and December 2009 in Nairobi, Kenya. Cervical cells for HPV DNA testing and conventional cervical cytology were collected. HPV types were detected and genotyped by Roche Linear Array PCR assay.

Results Among 283 women, the overall HPV prevalence was 62%, and 132 (47%) had ≥1 high-risk (HR)-HPV genotype. Of 268 women with cervical cytology results, 18 (7%) had high-grade cervical lesions or more severe by cytology, of whom 16 (89%) were HR-HPV-positive compared with 82 (41%) of 199 women with normal cytology (p<0.001). The most common HR-HPV types in women with a high-grade lesion or more severe by cytology were HPV-52 (44%), HPV-31 (22%), HPV-35 (22%), HPV-51 (22%) and HPV-58 (22%). HR-HPV genotypes HPV-16 or HPV-18 were found in 17% of women with high-grade lesions or more severe. HR-HPV screening applied in this population would detect 89% of those with a high-grade lesion or more severe, while 44% of women with normal or low-grade cytology would screen positive.

Conclusion HR-HPV prevalence was high in this population of HIV-infected women with an uninfected partner. Choice of screening for all HR genotypes versus a subset of HR genotypes in these HIV-infected women will strongly affect the performance of an HPV screening strategy relative to cytological screening. Regional and subpopulation differences in HR-HPV genotype distributions could affect screening test performance.

  • HPV
  • women
  • cervical cytology
  • cervical neoplasia
  • HIV

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  • Handling editor Francesca Ceccherini Silberstein

  • Contributors BG, AFR, CF, RB, RC, JK and JSS conceived and planned the study. RB and RC conducted study recruitment and collected the specimens. AFR, JAC, RB, RC and JSS contributed to sample preparation and conducted the assays. BG, AFR and JAC planned and carried out the analyses. BG wrote the manuscript with support from AFR, JAC and JSS. All authors provided critical feedback, helped shape the research, analysis and manuscript, and approved the final version to be published.

  • Funding Research support included National Institutes of Health (NIH) (R01 AI0684316 and R24 TW007988) from Fogarty International Center (FIC) through Vanderbilt University. In addition, CF received support from NIH (K24 AI087399), RB was a scholar at the University of Washington International AIDS Research and Training Program (IARTP) funded by FIC (D43 TW000007), and BG was supported by an NIH/FIC postdoctoral fellowship (3D43TW000007-22S1) and by an NIH/NIAID Career Development Award (K01AI098527). AFR was supported by an NIH/NICHD Career Development Award (K23HD071788). RC received support from the International Research Scientist Development Award (K01 TW008406). This publication was made possible with help from the University of Washington Center for AIDS Research (CFAR), an NIH-funded programme (P30 AI027757), and the University of North Carolina at Chapel Hill Center for AIDS Research (CFAR) (P30 AI050410), which are supported by the following NIH institutes and centres: NIAID, NCI, NIMH, NIDA, NICHD, NHLBI and NIA.

  • Disclaimer The content of this manuscript is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health, Fogarty International Center or Vanderbilt University.

  • Competing interests JSS has received unrestricted grants, research support or consultancy fees from Hologic, BD Corporation and Trovagene within the last 5 years.

  • Patient consent for publication Not required.

  • Ethics approval Written informed consent was obtained and ethical approval was granted by the Institutional Review Board (IRB) at the University of Washington (#30243) and the Ethics and Research Committee (ERC) at Kenyatta National Hospital (P25/2/2007).

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data availability statement Data are available upon reasonable request. Use of data is subject to approval of the Kenyatta National Hospital Ethics and Research Committee.