BACKGROUND: Despite HAART, the prevalence and incidence of anal cancer in HIV-infected individuals have increased. Recently, the relationship between the severity of cervical lesions and oncogenic HPV load was demonstrated; however, few studies have assessed the level and the significance of oncogenic HPV load in patients at risk for anal neoplasia. OBJECTIVES: To assess HPV genotypes and HPV 16/18 DNA load in HIV-1 infected patients at risk for anal neoplasia. STUDY DESIGN: Cross-sectional pilot study from male and female HIV-1 infected individuals at risk for anal neoplasia in an outpatient HIV Clinical Unit of Marseilles university Hospitals. RESULTS: Anal HPV was found in 79% of the patients whereas high-risk (HR) HPV types and infection with multiple HPV types were found in 83% and 61% of the patients, respectively. Using a sensitive real-time PCR, median HPV 16 and 18 DNA load were 5 x 10(6) copies/10(6) cells and 3.2 x 10(5) copies/10(6) cells, respectively. Notably, there were no significant differences in the HPV 16/18 viral loads with respect to the anoscopic results. CONCLUSIONS: Longitudinal studies are needed to evaluate the link between high anal HPV DNA load and progression to anal squamous intraepithelial lesions and anal cancer.
BACKGROUND: Despite HAART, the prevalence and incidence of anal cancer in HIV-infected individuals have increased. Recently, the relationship between the severity of cervical lesions and oncogenic HPV load was demonstrated; however, few studies have assessed the level and the significance of oncogenic HPV load in patients at risk for anal neoplasia. OBJECTIVES: To assess HPV genotypes and HPV 16/18 DNA load in HIV-1 infectedpatients at risk for anal neoplasia. STUDY DESIGN: Cross-sectional pilot study from male and female HIV-1 infected individuals at risk for anal neoplasia in an outpatient HIV Clinical Unit of Marseilles university Hospitals. RESULTS: Anal HPV was found in 79% of the patients whereas high-risk (HR) HPV types and infection with multiple HPV types were found in 83% and 61% of the patients, respectively. Using a sensitive real-time PCR, median HPV 16 and 18 DNA load were 5 x 10(6) copies/10(6) cells and 3.2 x 10(5) copies/10(6) cells, respectively. Notably, there were no significant differences in the HPV 16/18 viral loads with respect to the anoscopic results. CONCLUSIONS: Longitudinal studies are needed to evaluate the link between high anal HPV DNA load and progression to anal squamous intraepithelial lesions and anal cancer.
Authors: Maarten F Schim van der Loeff; Sofie H Mooij; Oliver Richel; Henry J C de Vries; Jan M Prins Journal: Curr HIV/AIDS Rep Date: 2014-09 Impact factor: 5.071
Authors: Celia M Limia; Yudira Soto; Yanara García; Orestes Blanco; Vivian Kourí; María V López; María E Toledo; Lissette Pérez; Yoanna Baños; Yaniris Caturla; Francisco Aguayo Journal: Infect Agent Cancer Date: 2017-01-17 Impact factor: 2.965
Authors: Melissa Agsalda-Garcia; Tiffany Shieh; Eleanore Chuang; Nicholas Loi; Cris Milne; Rui Fang; Eunjung Lim; Jeffrey Killeen; Bruce Shiramizu Journal: Int J Environ Res Public Health Date: 2018-08-08 Impact factor: 3.390