title: Human papillomavirus type in anal epithelial lesions is influenced by human immunodeficiency virus.
abstract: OBJECTIVE
  Infection with human immunodeficiency virus (HIV) increases the risk for human papillomavirus (HPV)-associated genital neoplasia. Human immunodeficiency virus-infected patients also have higher rates of treatment failure and more rapid neoplastic progression. Impaired immune function does not entirely explain these clinical observations. This pilot project was designed to investigate the hypothesis that HIV infection is associated with changes in HPV type and integration within anogenital lesions that could explain the increased risk of neoplastic progression.
  
  
  METHODS
  Anal neoplastic lesions from patients with and without HIV infection were analyzed for the presence, type, and integration status of HPV by colorimetric in situ hybridization. Tissue localization of HIV was evaluated by p24 immunohistochemistry and HIV-1 DNA polymerase chain reaction. Results for matched histology were compared for the two patient groups.
  
  
  RESULTS
  For all lesions, the presence of high-risk HPV types and multiple HPV types was strongly associated with HIV infection (P = .003 and .0003, respectively). For lesions with matched histology there was no association of HPV integration with HIV status. Tissue localization of HIV did not significantly influence HPV type or integration.
  
  
  CONCLUSIONS
  The presence of high-risk HPV types and multiple types within low-grade lesions may explain the increased risk of neoplastic progression in HIV patients. Colocalization of HIV and HPV does not appear to be required for this effect. There is no evidence that HPV integration is influenced by HIV infection.
authors.affiliation: Department of Pathology and Laboratory Medicine, Emory University, Atlanta, Ga., USA.
authors.forename: E R
authors.initials: ER
authors.lastname: Unger
authors.forename: S D
authors.initials: SD
authors.lastname: Vernon
authors.forename: D R
authors.initials: DR
authors.lastname: Lee
authors.forename: D L
authors.initials: DL
authors.lastname: Miller
authors.forename: S
authors.initials: S
authors.lastname: Sharma
authors.forename: K A
authors.initials: KA
authors.lastname: Clancy
authors.forename: C E
authors.initials: CE
authors.lastname: Hart
authors.forename: W C
authors.initials: WC
authors.lastname: Reeves
mesh_terms: D000293:Adolescent; D000328:Adult; D001005:Anus Neoplasms / Q000276:immunology / Q000473:pathology / Q000821:virology*; D002278:Carcinoma in Situ / Q000276:immunology / Q000473:pathology / Q000821:virology*; D002294:Carcinoma, Squamous Cell / Q000276:immunology / Q000473:pathology / Q000821:virology*; D003218:Condylomata Acuminata / Q000276:immunology / Q000473:pathology / Q000821:virology*; D004279:DNA, Viral / Q000032:analysis; D005260:Female; D016655:HIV Core Protein p24 / Q000032:analysis; D015658:HIV Infections / Q000150:complications* / Q000473:pathology; D015497:HIV-1 / Q000235:genetics / Q000276:immunology; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D008297:Male; D008875:Middle Aged; D027383:Papillomaviridae / Q000235:genetics / Q000302:isolation & purification; D030361:Papillomavirus Infections / Q000150:complications* / Q000473:pathology; D010865:Pilot Projects; D016133:Polymerase Chain Reaction; D014412:Tumor Virus Infections / Q000150:complications* / Q000473:pathology; D016662:Virus Integration
chemical_list: D004279:DNA, Viral; D016655:HIV Core Protein p24