Anal squamous intraepithelial lesions: Relation to HIV and human papillomavirus infection

Authors
Citation
Jm. Palefsky, Anal squamous intraepithelial lesions: Relation to HIV and human papillomavirus infection, J ACQ IMM D, 21, 1999, pp. S42-S48
Citations number
28
Categorie Soggetti
Clinical Immunolgy & Infectious Disease",Immunology
Journal title
JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY
ISSN journal
15254135 → ACNP
Volume
21
Year of publication
1999
Supplement
1
Pages
S42 - S48
Database
ISI
SICI code
1525-4135(19990801)21:<S42:ASILRT>2.0.ZU;2-M
Abstract
Studies from the era prior to the introduction of highly active antiretrovi ral therapy (HAART) have shown that the prevalence of anal infection with h uman papillomavirus (HPV) and anal squamous intraepithelial lesions (ASIL) were high among HIV-positive homosexual men, and to a lesser extent, among HIV-negative homosexual men. The data also show that the incidence of high- grade ASIL (HSIL), the putative invasive cancer precursor lesion, was high in these groups. Early data suggest that at least 75% of those with HSIL le sions do not regress while receiving HAART. Given that progression of HSIL to invasive cancer may require several years, lengthened survival associate d with HAART may paradoxically lead to an increased risk of anal cancer. Th e potential to prevent anal cancer through detection and treatment of anal HSIL suggests a need to screen high-risk individuals with anal cytology, si milar to cervical cytology screening to prevent cervical cancer. Cost-effec tiveness analyses suggest that anal screening programs may be cost-effectiv e in HIV-positive men. However, barriers to implementation of screening inc lude inadequate numbers of clinicians skilled in diagnosis and treatment of HSIL and lack of medical alternatives to surgical excision. Recent progres s in understanding the pathogenesis of ASIL in HIV-positive men points to a role for decreased cell-mediated immunity to HPV antigens as well as the e ffects of the HIV-1 tat protein in modulating the biology of HPV-infected k eratinocytes.