Treatment of HIV, rather than HIV immunosuppression, appears to play a role in oral HPV infections in HIV+ individuals.

Human immunodeficiency virus (HIV)-positive women may represent one of the fastest-growing populations at risk for acquiring cervical cancer and thus require frequent screening. The purpose of the present studies was to validate a PCR-based urine assay by comparing detection and genotyping of human papillomavirus (HPV) DNA in urine samples and matching cervical swab specimens of HIV-positive women. Despite a difference in amplifiability, the prevalence of any HPV genotype (58% for the cervical swab specimens and 48% for the urine specimens) was not significantly different in this population. The levels of concordance were 70, 71, and 78% for detection of any HPV type, any high-risk HPV type, or any low-risk HPV type in the two specimen types, respectively. While instances of discordant detection were greater for the cervical swab specimens than for the urine specimens, this was not statistically significant. The distributions of HPV genotypes were similar in the cervix and the urine for the majority of types examined. Importantly, detection of HPV DNA in urine was associated with an abnormal Papanicolaou smear to the same extent that detection of HPV DNA in a cervical swab specimen was. These data provide preliminary support for the proposal to use urine testing as a primary or secondary screening tool for cervical cancer in HIV-positive women or as an epidemiological tool. Additional studies with larger sample sizes must be conducted in order to further verify these findings. (25). Importantly, infection with HPV, even high-risk types, is asymptomatic in most people and usually does not lead to cancer. However, more than 35 HPV types have been found to be associated with at least 90% of cases of cervical intraepithelial neoplasia, which is a precursor lesion to cervical cancer (16,21).Although the medical standard for the diagnosis of HPV disease is the Papanicolaou (Pap) smear, screening by this type of method has inherent problems. Only 15 to 50% of patients with HPV infections are accurately identified by Pap smears (22,26). Additionally, the efficacy of screening by use of the Pap smear relies on repeated (yearly) visits. Approximately 10% of women in the United States have never had a Pap smear, and about 30% of women do not have them on a regular basis (1,2,3,29). Furthermore, Pap smear screening requires a pelvic examination, which is invasive and uncomfortable for the patient as well as time-consuming for the health care provider (27). Perhaps the use of urine sampling for routine detection of HPV could provide a preliminary screen for cervical cancer and thus circumvent the need for an annual Pap smear for women who are negative for HPV DNA. Alternatively, detection of HPV DNA in urine could possibly function as a secondary screening technique for cervical cancer in that it could be used to triage women with atypical squamous cells of undetermined significance (ASCUS).Methods for the detection of DNA in patient urine have recently been used to diagnose other common STDs that affect the cervix, such as...

Prevalence of 27 human papillomavirus (HPV) genotypes was assessed in 1,331 women in three clinical settings: Family planning clinic (low-risk HIV-, n = 202, 21.3% HPV+), colposcopy clinic (high-risk HIV-, n = 854, 34.3% HPV+), and HIV outpatient clinic (HIV+, n = 275, 48.7% HPV+). Compared to women from both family planning and colposcopy clinics, HIV+ women revealed significantly higher prevalence of infection with oncogenic, non-oncogenic, and multiple HPV types. HPV types 52 and 51 were most prevalent in the low-risk HIV- women, whereas in the high-risk HIV- women, HPV types 16, 52, 58, and 35 were most prevalent. Interestingly, in the HIV+ women, less characterized types 83, 53, and 54 were most prevalent. The distinct profiles of genotype prevalence persisted after stratification by Pap smear status. After adjustment for concurrent infections with other types, HPV type 51 in the low-risk HIV- women, and types 16, 35, 39, 45, 52, and 58 in the high-risk HIV- women were significantly associated with cytologic abnormalities (exact P < 0.05). In HIV+ women across CD4 cell count strata, HPV types 42, 16, and 82 revealed significant decreasing trends with increasing CD4 counts (exact P for trend < 0.05). These data suggest distinct genotypic prevalence profiles in women at diverse risk for cervical cancer. The association of several genotypes with cytologic abnormalities underscores the need for vaccines targeting a wide range of HPV types.

The prevalence of human papillomavirus type 16 E6 variant lineages was characterized in a cross-sectional study of 24 human immunodeficiency virus type 1 (HIV)-positive and 33 HIV-negative women in New Orleans. The European prototype was the predominant variant in the HIV-negative women (39?4 %), while in the HIV-positive women the European 350G variant was predominant (29?1 %). In exact logistic regression models, HIV-positive women were significantly more likely to harbour any variant with a nucleotide G-350 mutation compared with HIV-negative women [58?3 % vs 21?1 %; adjusted odds ratio (AOR)=6?28, 95 % confidence interval (CI) =1?19-46?54]. Models also revealed a trend towards increased prevalence of Asian-American lineage in HIV-positive women compared with HIV-negative women (25?0 % vs 6?0 %; AOR=6?35,. No association was observed between any variant and cytology or CD4 cell counts or HIV-1 viral loads. These observations reflect a difference in the distribution of HPV-16 variants among HIV-positive and -negative women, indicating that HIV-positive status may lead to increased prevalence of a subset of variants.Human papillomavirus (HPV) type 16 is the most prevalent genital HPV type and accounts for~50 % of cervical cancer cases worldwide Yamada et al., 1997;Munoz et al., 2003). In spite of high prevalence and robust associations with cervical cancer, the majority of HPV-16 infections are transient and only a fraction progress to develop pre-invasive and invasive lesions (Walboomers et al., 1999), underscoring the interplay of additional factors in development of cervical cancer (Munoz et al., 1992;Hildesheim et al., 2001a;Moreno et al., 1995) such as behavioural (smoking, parity, oral contraceptive use) (Castellsague et al., 2002), host genetic (HLA phenotypes and p53 polymorphisms) (Giannoudis & Herrington, 2001;Hildesheim & Wang, 2002;Maciag & Villa, 1999) and viral factors (HPV genotypes, intratype variants and viral load) (Hildesheim & Wang, 2002; Londesborough et al., 1996; Lorincz et al., 1992Lorincz et al., , 2002. HPV variants are defined by 0-2 % sequence heterogeneity in the L1, L2 and E6 genes (Yamada et al., 1995). HPV-16 intratype variants have been shown in molecular studies to have altered oncogenic potential (Stoppler et al., 1996). Several epidemiological studies have corroborated this difference in oncogenic potential, specifically for the non-European variants (Hildesheim et al., 2001b;Xi et al., 1997), European 350G variants (Andersson et al., 2000Zehbe et al., 1998Zehbe et al., , 2001 Kammer et al., 2002) and the Asian-American lineages (Berumen et al., 2001). This difference in oncogenic potential could be attributed to one or a combination of the following: (i) increased infectivity and/or increased virus persistence; (ii) increased ability to cause immortalization of cervical epithelial cells; or (iii) increased ability to escape immune surveillance.The cell-mediated immune system is believed to be central to the control of HPV infection, as evidenced by an increase in the in...

The primary risk factor for cervical cancer is infection with high-risk genotypes of human papillomavirus (HPV). This study compared HPV DNA detection between cervical swabs (CX) and self-administered vaginal swabs (SV). Phase I participants were 199 women chosen from a study comparing the detection of Chlamydia trachomatis from various anogenital sites. Phase II participants were 135 women from either the Colposcopy or HIV Outpatient Clinic. HPV DNA testing was performed using polymerase chain reaction and Roche reverse line blot hybridization. In Phase I samples, more CX samples amplified and more HPV genotypes (P < 0.05) were detected in CX. Genotype 52 were seen more in the cervix, whereas genotype 82 (MM4) was detected solely in the vagina. The presence of high-risk HPV genotypes in the cervix was a predictor of an abnormal Papanicolaou (Pap) smear. In Phase II samples, CX samples amplified more, but similar rates of HPV genotypes were seen in SV and CX samples. Higher concordance rates of high-risk genotypes were seen in Phase II compared to Phase I samples. Phase II demonstrated the feasibility of utilizing SV sampling to reflect cervical status. If validated, a self-vaginal swab method to detect cervical HPV DNA status could be utilized to triage women with indeterminate Pap smears and be a useful method to collect epidemiological data from large populations.