Kovacic Melinda Butsch, Castle Philip E, Herrero Rolando, Schiffman Mark, Sherman Mark E, Wacholder Sholom, Rodriguez Ana C, Hutchinson Martha L, Bratti M Concepción, Hildesheim Allan, Morales Jorge, Alfaro Mario, Burk Robert D
Division of Cancer Epidemiology and Genetics and Cancer Prevention Fellowship Program, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA.
Cancer Res. 2006 Oct 15;66(20):10112-9. doi: 10.1158/0008-5472.CAN-06-1812.
Persistent cervical infections with carcinogenic human papillomaviruses (HPV) cause virtually all cervical cancer. Cytologic abnormalities are the manifestations of HPV infections used to identify women at risk. To compare the potential of the full range of anogenital HPV genotypes to induce cytopathic effects, we examined the influences of HPV type, viral load, and age on cytopathology among 1,222 women having a single HPV type at enrollment into a 10,000-woman population-based study in Costa Rica. Cervical specimens were tested for approximately 40 HPV types by MY09/MY11 L1 primer PCR and type-specific dot blot hybridization. Types were organized by phylogenetic species and cancer risk. PCR signal strength served as a qualitative surrogate for viral load. Overall, 24.8% [95% confidence interval (95% CI), 22.4-27.3] of single prevalent HPV infections had concurrent abnormalities (atypical squamous cells or worse) ranging from 0.0% to 80.0% based on HPV type. Noncarcinogenic alpha3/alpha15 types, although highly prevalent, uncommonly caused cytologic abnormalities (13.1%; 95% CI, 9.8-17.0). In contrast, one quarter to nearly one half of infections with a single major carcinogenic species type (alpha9/alpha11/alpha7/alpha5/alpha6) produced abnormalities. Greater abnormalities were observed with increasing qualitative viral load of carcinogenic types; fewer abnormalities were observed among older women (>54 years). A high percentage (46.2%) of detected abnormalities in women infected with HPV16 or related alpha9 types were high grade or worse, consistent with strong carcinogenicity, compared with 10.7% in women infected with alpha7 types, including HPV18, a major cause of adenocarcinoma. The lack of evident severe abnormalities associated with HPV18 and related HPV types might have implications for screening for poorly detected glandular and alpha7-related lesions.
致癌性人乳头瘤病毒(HPV)持续感染子宫颈几乎会引发所有的子宫颈癌。细胞学异常是HPV感染的表现形式,可用于识别有风险的女性。为了比较所有肛门生殖器HPV基因型诱导细胞病变效应的潜力,我们在哥斯达黎加一项基于10000名女性的人群研究中,对1222名单一HPV感染类型的女性进行了研究,探讨HPV类型、病毒载量和年龄对细胞病理学的影响。通过MY09/MY11 L1引物PCR和型特异性斑点杂交检测宫颈标本中的约40种HPV类型。根据系统发育种类和致癌风险对这些类型进行分类。PCR信号强度作为病毒载量的定性替代指标。总体而言,24.8%[95%置信区间(95%CI),22.4 - 27.3]的单一流行HPV感染同时存在异常(非典型鳞状细胞或更严重病变),根据HPV类型不同,异常比例从0.0%到80.0%不等。非致癌性的α3/α15类型虽然感染率很高,但很少引起细胞学异常(13.1%;95%CI,9.8 - 17.0)。相比之下,单一主要致癌种类类型(α9/α11/α7/α5/α6)的感染中有四分之一到近一半会产生异常。致癌类型的定性病毒载量越高,观察到的异常越多;年龄较大(>54岁)的女性中观察到的异常较少。与α7类型(包括HPV18,腺癌的主要病因)感染的女性相比,感染HPV16或相关α9类型的女性中检测到的异常有很高比例(46.2%)为高级别或更严重病变,这与强致癌性一致。与HPV18及相关HPV类型相关的明显严重异常的缺乏,可能对筛查难以检测到的腺性和α7相关病变有影响。