Article

Prevalence and Persistence of Cervical Human Papillomavirus Infection In HIV-Positive Women Initiating Highly-Active Antiretroviral Therapy

Department of Medicine, Indiana University School of Medicine, Indianapolis, IN 46202-5124, USA.
JAIDS Journal of Acquired Immune Deficiency Syndromes (Impact Factor: 4.56). 05/2009; 51(3):274-82. DOI: 10.1097/QAI.0b013e3181a97be5
Source: PubMed

ABSTRACT

To determine the prevalence of human papillomavirus (HPV) DNA in cervical specimens from treatment-naive women initiating highly active antiretroviral therapy (HAART) and explore the longitudinal association of HPV DNA with CD4 count and HIV viral load (VL).
Women enrolled before HAART were evaluated at baseline, weeks 24, 48, and 96 with CD4 count, VL, and cervical swab for HPV DNA.
The 146 subjects had a median CD4 count of 238 cells per microliter and VL of 13,894 copies per milliliter. Ninety-seven subjects (66%) had HPV DNA detected in the baseline specimen including 90 subjects (62%) positive for 1 or more high-risk HPV types. HPV DNA detection declined to 49% at week 96 and that of a high risk HPV type to 39%. The duration of follow-up was associated with decreased detection of HPV DNA of any type (P = 0.045) and of high-risk HPV types (P = 0.003). There was at most a marginal association between HAART response and loss of detection of cervical HPV DNA.
Women initiating HAART had a high prevalence of cervical HPV DNA that declined over 96 weeks of HAART. The relationship of CD4 count and VL response to the decline of cervical HPV DNA was not strong.

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Available from: Darron Brown, Feb 03, 2014
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    • "This assay detects 37 HPV types using nondegenerate, 5′ biotin– labeled primer pools for polymerase chain reaction amplification within the L1 region of the HPV genome. Reactions were amplified in a PerkinElmer TC9600 Thermal Cycler as previously described [24] . A positive control reaction (sample provided by Roche Molecular Diagnostics) and a negative control reaction (no DNA) were performed with each assay. "
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    ABSTRACT: Background: Persistent infection with oncogenic human papillomavirus (HPV) is associated with an increased risk of cervical malignancy. Redetection of type-specific HPV after a period of nondetection may be caused by reactivation of a low-level persistent infection. Little is known about factors associated with type-specific HPV redetection. Methods: For a longitudinal cohort of adolescent women with frequent behavioral and sexually transmitted infection (STI) information (every 3 months), Cox proportional hazard models were used to assess the influence of sexual behaviors and STIs on the redetection of oncogenic or high-risk HPV infections. Results: A total of 210 type-specific high-risk HPV detection episode periods were identified in this longitudinal cohort; 71 (33.8%) were characterized by a period of nondetection followed by redetection. Chlamydia trachomatis (hazard ratio [HR], 3.14; 95% confidence interval [CI], 1.44-6.86) was associated with redetection; redetection was >2 times more likely with each additional self-reported sex partner in the past 3 months (HR, 2.26; 95% CI, 1.35-3.78). Conclusions: This study demonstrates the role of C. trachomatis and number of recent sexual partners in type-specific HPV redetection. Given that persistent oncogenic HPV infections are associated with cancer-related outcomes, understanding the potential role of such factors in the pathogenesis of HPV-related outcomes is important.
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    • "The HIV Epidemiology Research Study (HERS), a U.S. observational, multisite cohort study, among women with preexisting abnormal cervical cytology, ART was associated with enhanced HPV clearance but not with regression of abnormal Pap results (Paramsothy et al. 2009). In a study of women initiating HAART there was a high prevalence of cervical HPV DNA at baseline, but this declined over 96 weeks of HAART (Fife et al. 2009). On the other hand, with 15 months of follow-up, persistence of high-risk HPV and progression of SIL were comparable among women without antiretroviral treatment, those treated with nucleoside analogues only, and those treated with ART (Lillo 2001). "

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