Little is known about the interaction between human papillomavirus (HPV) and HIV. This study aimed to explore the association of oncogenic (high risk) and nononcogenic (low risk) HPV with HIV incidence.
We used 1683 urethral swabs collected at the last follow-up visit of a male circumcision trial conducted in Orange Farm (South Africa). Swabs analyses and HPV genotyping were performed by polymerase chain reaction. We estimated HIV adjusted incidence rate ratios (aIRRs) and 95% confidence intervals (CIs) using survival analysis. Background characteristics, male circumcision status, sexual behavior, HPV status, and other sexually transmitted infections were used as covariates.
The prevalence of HR and LR HPV was 14.0% (95% CI: 12.4 to 15.7) and 17.3% (95% CI: 15.6 to 19.2), respectively. When controlling for HR-HPV status, LR-HPV status was not associated with HIV incidence (aIRR = 1.13, 95% CI: 0.40 to 3.16; P = 0.82). When controlling for all covariates, HIV incidence increased significantly with HR-HPV positivity (aIRR = 3.76, 95% CI: 1.83 to 7.73, P < 0.001) and with the number of HR-HPV genotypes (adjusted-P linear trend = 0.0074).
Several explanations could account for our findings. One is that HR-HPV facilitates HIV acquisition. The association of HPV with HIV acquisition requires further investigations.
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"Among the HPV types currently considered oncogenic, HPV-16 and HPV-18 are the most common cumulatively accounting for over 70% of cervical cancer cases worldwide . There appears to be an association between human immunodeficiency virus (HIV) and HPV infection      , with the cervical cancer and HIV infection epidemics having a strong geographic correlation in sub-Saharan Africa. There are an estimated 22.5 million people living with HIV in sub-Saharan Africa, representing 68% of Fig. 1. "
[Show abstract][Hide abstract] ABSTRACT: In developing countries, risk of human papillomavirus (HPV) infection may be increased by the high prevalence of human immunodeficiency virus (HIV) infection. We evaluated the safety and immunogenicity of the HPV-16/18 AS04-adjuvanted vaccine in HIV-infected women in South Africa. Asymptomatic HIV-positive women aged 18-25 years (N=120) were stratified by CD4(+) T-cell count and randomised (1:1) to receive HPV-16/18 vaccine (Cervarix(®); GlaxoSmithKline Vaccines) or placebo (Al[OH]3) at 0, 1 and 6 months (double-blind). HIV-negative women (N=30) received HPV-16/18 vaccine (open label). Anti-HPV-16/18 antibody and CD4(+) T-cell responses, CD4(+) T-cell count, HIV viral load, HIV clinical stage and safety were evaluated for 12 months. The safety and reactogenicity profile of the HPV-16/18 vaccine was comparable in HIV-positive and HIV-negative women. Irrespective of baseline HPV status, all HIV-positive and HIV-negative women who received the HPV-16/18 vaccine were seropositive for both HPV-16 and HPV-18 after the second vaccine dose (month 2) and remained seropositive for both antigens at month 12. Anti-HPV-16/18 antibody titres at month 12 remained substantially above levels associated with natural infection. The HPV-16/18 vaccine induced sustained anti-HPV-16/18 CD4(+) T-cell responses in both HIV-positive and HIV-negative women. No impact of baseline CD4(+) T-cell count or HIV viral load was observed on the magnitude of the immune response in HIV-positive women. In HIV-positive women, CD4(+) T-cell count, HIV viral load and HIV clinical stage were unaffected by HPV-16/18 vaccine administration. In conclusion, the HPV-16/18 AS04-adjuvanted vaccine appears immunogenic and well-tolerated in women with HIV infection. Study ID: 107863/NCT00586339.
"It is well established that HIV-infected men and women are at increased risk of anogenital HPV infection; yet, until recently, little was known about the potential role of HPV infection in HIV acquisition. Recent studies suggest that infection with various HPV subtypes, both oncogenic and nononcogenic, is ass-ociated with increased risk of HIV acquisition in men and women      . One explanation for the association is that cervical procedures performed as part of the evaluation and treatment of HPV-induced cervical dysplasia provide a portal of HIV entry due to disruption of the normal mucosal ISRN Obstetrics and Gynecology barrier. "
[Show abstract][Hide abstract] ABSTRACT: Objective. Cervical human papillomavirus (HPV) infection has been associated with human immunodeficiency virus (HIV) acquisition in populations with a high prevalence of both infections. Procedures performed in the management of cervical dysplasia may facilitate HIV entry via mechanical injury. We sought to investigate the association between cervical procedures and incident HIV. Methods. Data on cervical cancer screening and procedures were collected in a cohort study evaluating the diaphragm for HIV prevention in 2040 women. In this secondary analysis, we investigated the association between cervical procedures and HIV acquisition. Results. Out of 2027 HIV-negative women at baseline, 199 underwent cervical procedures. Cumulative risk of HIV was 4.3% over 21 months of median followup (n = 88). Compared with women without cervical procedures, we observed no difference in HIV incidence after a cervical biopsy (RR 0.92, 95% CI 0.39-2.16), endocervical curettage (RR 0.29, 95% CI 0.07-1.22), or loop electrosurgical excision procedure (RR 1.00, 95% CI 0.30-3.30). Conclusions. In this cohort, cervical procedures were not associated with HIV incidence. This lack of association could be due to the small number of events.
ISRN obstetrics and gynecology 11/2011; 2011(16):789106. DOI:10.5402/2011/789106
"After alignment using the SeqScape v2.5 software (Applied Biosystems), sequences were analysed in GenBank by using the NCBI BLAST tool. The risk level of each genotype was classified according to oncogenic properties in the cervix . "
[Show abstract][Hide abstract] ABSTRACT: A study including 166 subjects was performed to investigate the frequency and persistence over a 6-month interval of concurrent oral and anal Human Papillomavirus (HPV) infections in Human Immunodeficiency Virus (HIV)-infected men who have sex with men (MSM).
Patients with no previously documented HPV-related anogenital lesion/disease were recruited to participate in a longitudinal study. Polymerase chain reaction (PCR) was performed to detect HPV from oral and anal swabs and to detect Human Herpes Virus 8 (HHV-8) DNA in saliva on 2 separate specimen series, one collected at baseline and the other collected 6 months later. A multivariate logistic analysis was performed using anal HPV infection as the dependent variable versus a set of covariates: age, HIV plasma viral load, CD4+ count, hepatitis B virus (HBV) serology, hepatitis C virus (HCV) serology, syphilis serology and HHV-8 viral shedding. A stepwise elimination of covariates with a p-value > 0.1 was performed.
The overall prevalence of HPV did not vary significantly between the baseline and the follow-up, either in the oral (20.1 and 21.3%, respectively) or the anal specimens (88.6 and 86.3%). The prevalence of high-risk (HR) genotypes among the HPV-positive specimens was similar in the oral and anal infections (mean values 24.3% and 20.9%). Among 68 patients with either a HR, low-risk (LR) or undetermined genotype at baseline, 75% had persistent HPV and the persistence rates were 71.4% in HR infections and 76.7% in LR infections. There was a lack of genotype concordance between oral and anal HPV samples. The prevalence of HR HPV in anus appeared to be higher in the younger patients, peaking (> 25%) in the 43-50 years age group. A decrease of the high level of anal prevalence of all genotypes of HPV in the patients > 50 years was evident. HHV-8 oral shedding was positively related to HPV anal infection (p = 0.0046). A significant correlation was found between the persistence of HHV-8 shedding and HIV viral load by logistic bivariate analysis (Odds Ratio of HHV-8 persistence for 1-log increase of HIV viral load = 1.725 ± 0.397, p = 0.018).
A high prevalence of HPV infection was found in our cohort of HIV-infected MSM, with a negative correlation between anal HPV infection and CD4 cell count.