Rosales-Terrazas Estrella, Ramirez-Amador Velia, Garcia-Carranca Alejandro, Guido-Jimenez Miriam, Irigoyen-Camacho Esther, Ortiz-Sanchez Elizabeth and Anaya-Saavedra Gabriela
Background: In HIV-patients, a proportion of benign HPV-associated oral lesions (HPV-OLs) contain high risk- HPV (HR-HPV) sequences. Recent studies demonstrated a p16INK4a overexpression in HPV-induced cancer and dysplastic lesions through pRB degradation by the E7-HPV oncoprotein; so, it has been considered a surrogate marker of HR-HPV oncogenic activity.
Objective: To establish the p16INK4a expression in HPV-OL from HIV-infected patients. Materials and method: A cross-sectional study was conducted in three HIV/AIDS referral centers in Mexico City. We performed histopathological diagnosis, HPV-DNA amplification, direct sequencing, and p16INK4a immunohistochemical staining in HPV-OLs. The U-Mann-Whitney, X2, and Fisher’s exact tests were used to determine the association between variables.
Result: In a total of 849 adult HIV-individuals examined, we found 29 (3.4%) patients with HPV-OLs, being multifocal epithelial hyperplasia (51.7%) the most common. Low-risk-HPV (LR-HPV) types were identified in 82.7% and HR-HPV in 10.3%. HPV-OLs exhibited a moderate/strong but only nuclear p16INK4a immunoexpression; no correlation between p16INK4a expression and HPV type were found.
Conclusion: In HPV-OLs from HIV-infected patients, the comparable p16INK4a immunoexpression, independently of the specific HPV-type, as well as the absence of cytoplasmic staining, may suggest a lack of HR-HPV activity. Longitudinal studies based on oncogenic viral gene expression are warranted.
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