HUMAN-PAPILLOMAVIRUS TYPE IN ANAL EPITHELIAL LESIONS IS INFLUENCED BYHUMAN-IMMUNODEFICIENCY-VIRUS

Citation
Er. Unger et al., HUMAN-PAPILLOMAVIRUS TYPE IN ANAL EPITHELIAL LESIONS IS INFLUENCED BYHUMAN-IMMUNODEFICIENCY-VIRUS, Archives of pathology and laboratory medicine, 121(8), 1997, pp. 820-824
Citations number
31
Categorie Soggetti
Pathology,"Medical Laboratory Technology","Medicine, Research & Experimental
Journal title
Archives of pathology and laboratory medicine
ISSN journal
00039985 → ACNP
Volume
121
Issue
8
Year of publication
1997
Pages
820 - 824
Database
ISI
SICI code
0003-9985(1997)121:8<820:HTIAEL>2.0.ZU;2-X
Abstract
Background and Objective.-Infection with human immunodeficiency virus (HIV) increases the risk for human papillomavirus (HPV)-associated gen ital neoplasia. Human immunodeficiency virus-infected patients also ha ve higher rates of treatment failure and more rapid neoplastic progres sion. Impaired immune function does not entirely explain these clinica l observations. This pilot project was designed to investigate the hyp othesis 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 fro m patients with and without HIV infection were analyzed for the presen ce, type, and integration status of HPV by colorimetric in situ hybrid ization. Tissue localization of HIV was evaluated by p24 immunohistoch emistry and HIV-1 DNA polymerase chain reaction. Results for matched h istology were compared for the two patient groups. Results.--For all l esions, the presence of high-risk HPV types and multiple HPV types was strongly associated with HIV infection (P = .003 and .0003, respectiv ely). For lesions with matched histology there was no association of H PV integration with HIV status. Tissue localization of HIV did not sig nificantly influence HPV type or integration. Conclusions.--The presen ce of high-risk HPV types and multiple types within low-grade lesions may explain the increased risk of neoplastic progression in HIV patien ts. Colocalization of HIV and HPV does not appear to be required for t his effect. There is no evidence that HPV integration is influenced by HIV infection.