title: Human papillomavirus HPV-16, 18, 52 and 58 integration in cervical cells of HIV-1-infected women.
abstract: BACKGROUND
  Genomic integration of high-risk human papillomavirus into the cellular genome is considered an important event in the pathogenesis of cervical cancer related to the progression from premalignant cervical lesions to invasive cervical carcinoma.
  
  
  OBJECTIVE
  This cross-sectional study was aimed to characterize the viral integration of HPV-16, HPV-18, HPV-52 and HPV-58 in cervical cells.
  
  
  METHODS
  HPV genotypes were determined by PCR and HPV integration by multiplex PCR in HIV-1-infected women without a background of HPV-related pathology.
  
  
  RESULTS
  This study included 251 cervical cells samples of consecutive HIV-positive women who were visited between 1999 and 2003. The overall prevalence of HPV infection was 53% (133/251, 95%CI: 47-59%). The most prevalent genotypes were HPV-16 (27%), HPV-33 (15%), HPV-52 (8%) and HPV-58 (8%). The prevalence of abnormal cervical cytology was 33% (83/251, 95%CI: 27-39%). The overall prevalence of HPV integration was 11% (27/251, 95%CI: 7-15%), and the prevalence of HPV-16 integration was 33% (22/67, 95%CI: 22-45%), HPV-18 integration was 30% (3/10, 95%CI: 7-65%) and HPV-52 integration was 10% (2/19, 95%CI: 1-32%). No HPV-58 integration was detected. The percentage of HPV-16 and HPV-18 integration increased with the severity of the cervical lesions, HPV-16 integration was almost 70% and HPV-18 integration was 50% in high-grade squamous intraepithelial lesions. Integration was the most important risk factor associated with cervical dysplasia (OR=30.6, 95%CI: 3.5-270.6).
  
  
  CONCLUSIONS
  HPV integration might represent a good biomarker of the evolution from HPV infection to cervical cancer. Further prospective studies are required to validate our findings.
authors.affiliation: Retrovirology Laboratory IrsiCaixa, Spain. PCC@general-lab.com
authors.forename: M P
authors.initials: MP
authors.lastname: Cañadas
authors.forename: S
authors.initials: S
authors.lastname: Videla
authors.forename: L
authors.initials: L
authors.lastname: Darwich
authors.forename: A
authors.initials: A
authors.lastname: Tarrats
authors.forename: M
authors.initials: M
authors.lastname: Piñol
authors.forename: F
authors.initials: F
authors.lastname: García-Cuyás
authors.forename: M
authors.initials: M
authors.lastname: Llatjos
authors.forename: C
authors.initials: C
authors.lastname: Alcalde
authors.forename: I
authors.initials: I
authors.lastname: Fernández
authors.forename: G
authors.initials: G
authors.lastname: Sirera
authors.forename: B
authors.initials: B
authors.lastname: Clotet
mesh_terms: D000328:Adult; D002584:Cervix Uteri / Q000821:virology*; D003430:Cross-Sectional Studies; D004279:DNA, Viral / Q000235:genetics* / Q000302:isolation & purification; D004847:Epithelial Cells / Q000821:virology*; D005260:Female; D015658:HIV Infections / Q000150:complications*; D006801:Humans; D027383:Papillomaviridae / Q000235:genetics / Q000302:isolation & purification*; D030361:Papillomavirus Infections / Q000453:epidemiology* / Q000821:virology; D016133:Polymerase Chain Reaction; D015995:Prevalence; D016662:Virus Integration
chemical_list: D004279:DNA, Viral