Strickler Howard D, Palefsky Joel M, Shah Keerti V, Anastos Kathryn, Klein Robert S, Minkoff Howard, Duerr Ann, Massad L Stewart, Celentano David D, Hall Charles, Fazzari Melissa, Cu-Uvin Susan, Bacon Melanie, Schuman Paula, Levine Alexandra M, Durante Amanda J, Gange Stephen, Melnick Sandra, Burk Robert D
Department of Epidemiology and Social Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
J Natl Cancer Inst. 2003 Jul 16;95(14):1062-71. doi: 10.1093/jnci/95.14.1062.
Human papillomavirus (HPV) type 16 is etiologically associated with approximately half of all cervical cancers. It is important, therefore, to determine the characteristics that distinguish HPV16 from other HPV types. A preliminary result based on cross-sectional baseline data in the Women's Interagency Human Immunodeficiency Virus (HIV) Study (WIHS) suggested that the prevalence of HPV16 might have a weaker association with immune status in HIV-seropositive women than that of other HPV types. To address this issue, we examined HPV test results from repeated study visits in the WIHS and from an independent study, the HIV Epidemiology Research Study (HERS).
HIV-seropositive women in the WIHS (n = 2058) and in the HERS (n = 871) were assessed semiannually. HPV DNA was detected in cervicovaginal lavage specimens by using polymerase chain reaction assays. Prevalence ratios were used to compare the prevalence of each HPV type in women with the lowest CD4+ T-cell counts (<200 T cells/mm3) with that of women with the highest CD4+ T-cell counts (> or =500 T cells/mm3). A summary prevalence ratio for each HPV type (i.e., across visits and studies) was estimated using generalized estimating equations. The association of CD4+ T-cell stratum with type-specific HPV incidence was measured using multivariable Cox regression models. All statistical tests were two-sided.
The prevalence ratio for HPV16 was low compared with that of other HPV types at every study visit in both cohorts. The generalized estimating equation summary prevalence ratio for HPV16 (1.25, 95% confidence interval [CI] = 0.97 to 1.62) was the smallest measured, and it was statistically significantly lower than that of all other HPV types combined (P =.01). The association of CD4+ T-cell stratum with HPV16 incidence was also among the smallest measured (hazard ratio = 1.69, 95% CI = 1.01 to 2.81).
The prevalent and incident detection of HPV16 is more weakly associated with immune status in HIV-seropositive women than that of other HPV types, suggesting that HPV16 may be better at avoiding the effects of immune surveillance, which could contribute to HPV16's strong association with cervical cancer.
16型人乳头瘤病毒(HPV)在约一半的宫颈癌病因学中发挥作用。因此,确定16型HPV与其他HPV类型相区别的特征非常重要。基于女性机构间人类免疫缺陷病毒(HIV)研究(WIHS)的横断面基线数据得出的初步结果表明,在HIV血清阳性女性中,16型HPV的流行率与免疫状态的关联可能比其他HPV类型弱。为解决这一问题,我们检查了WIHS重复研究访视以及一项独立研究——HIV流行病学研究(HERS)中的HPV检测结果。
对WIHS(n = 2058)和HERS(n = 871)中的HIV血清阳性女性每半年进行一次评估。通过聚合酶链反应检测宫颈阴道灌洗标本中的HPV DNA。患病率比用于比较CD4 + T细胞计数最低(<200个T细胞/mm3)的女性与CD4 + T细胞计数最高(≥500个T细胞/mm3)的女性中各型HPV的患病率。使用广义估计方程估计每种HPV类型(即跨访视和研究)的汇总患病率比。使用多变量Cox回归模型测量CD4 + T细胞分层与型特异性HPV发病率的关联。所有统计检验均为双侧检验。
在两个队列的每次研究访视中,16型HPV的患病率比均低于其他HPV类型。16型HPV的广义估计方程汇总患病率比(1.25,95%置信区间[CI] = 0.97至1.62)是所测量的最小值,并且在统计学上显著低于所有其他HPV类型的总和(P = 0.01)。CD4 + T细胞分层与16型HPV发病率的关联在所测量的结果中也处于最小之列(风险比 = 1.69,95% CI = 1.01至
2.81)。
在HIV血清阳性女性中,16型HPV的流行率和发病率与免疫状态的关联比其他HPV类型更弱,这表明16型HPV可能更善于避免免疫监视的影响,这可能有助于解释16型HPV与宫颈癌的强关联。