MOLECULAR EPIDEMIOLOGY OF PERSISTENT HPV INFECTION

描述：(改编自《调查者摘要》)1993年作者 开始了对人类自然历史的流行病学队列研究 低收入人群中人乳头瘤病毒感染与宫颈肿瘤的关系 巴西圣保罗的收入女性，世界上风险最高的地区之一 治疗宫颈癌。这项研究旨在回答以下问题 尚未在该肿瘤的流行病学调查中得到解决 疾病。尽管很少有人会质疑HPV感染是一种重要的 宫颈癌的病因，大多数流行病学数据都来自 回溯性研究，这些研究没有提供关于 同一个体宫颈HPV感染。巴西的队列研究 正在检验一种假设，即持续感染致癌性HPV 类型更有可能是导致宫颈病变的真正先兆事件 致癌。持续的感染正在记录的基础上 HPV的分子变体，这提供了更精细的细节水平 不仅仅是简单的HPV分型，可能还会揭开持久性本身的面纱 宫颈病变进展的其他预后标志物 损伤。 到1996年2月，这项研究将吸引2000名女性受试者。科目 每隔4年在预定退货中进行5年的跟踪 个月，第一年，此后每年一次，总共8个月 访问时间如下：初始、4、8、12、24、36、48和60个月。在每一个中 在这些访问中，受试者接受基于问卷的采访， 取宫颈样本进行巴氏细胞学和HPV检测，并抽血 为进行HPV抗体血清学检测而抽取的样本。宫颈造影术 第一年做一次，24个月和48个月。 考虑到宫颈癌对公共健康和经济的重要性 筛选，并考虑到目前联邦政府内部的动力 检查HPV检测在加强现有筛查方面的效用 计划，调查人员认为，显然有必要 对这一自然历史的长期多学科研究 恶性疾病。简而言之，这项正在进行的调查将进一步 从中医治法认识宫颈肿瘤的发病机制 以下是具体目标：(1)研究艾滋病的患病率和发病率 无症状妇女宫颈HPV一过性和持续性感染； 为了验证持续感染HPV会增加低风险的假设 分级和高度宫颈病变；(3)寻找流行病学 宫颈HPV持续感染的决定因素；(4)寻找 可能与HPV致癌类型相关的特定分子变异 宫颈癌变风险增加；(5)验证假设 宫颈病毒载量的测量可能与 持续感染和低、高级别皮损；(6)研究 人乳头瘤病毒衣壳抗原的体液免疫应答 宫颈HPV感染的持续性和进展的可能性 损伤严重程度。

DESCRIPTION: (Adapted from Investigator's Abstract) In 1993 the authors began an epidemiologic cohort study of the natural history of human Papillomavirus (HPV) infection and cervical neoplasia in a population of low income women in Sao Paulo, Brazil, one of the highest risk areas worldwide for cervical cancer. This study was designed to answer questions that have not yet been addressed in epidemiologic investigations of this neoplastic disease. Although few would dispute that HPV infection is an important cause of cervical cancer, most of the epidemiologic data have come from retrospective studies, which do not provide information on the dynamics of cervical HPV infection in the same individual. The Brazilian cohort study is testing the hypothesis that persistent infections with oncogenic HPV types are more likely to be the true precursor events leading to cervical carcinogenesis. Persistence of infections is being documented on the basis of molecular variants of HPV, which provides a much finer level of detail than simple HPV typing and may unveil in addition to persistence per se other prognostic markers of progression across the spectrum of cervical lesions. The study will accrue 2000 female subjects through February 1996. Subjects are being followed up over a 5 year period in scheduled returns every 4 months, in the first year, and once yearly thereafter, for a total of 8 visits as follows: initial, 4, 8, 12, 24, 36, 48, and 60 months. In each of these visits, subjects are submitted to a questionnaire-based interview, have a cervical specimen taken for Pap cytology and HPV testing, and a blood sample drawn for serologic testing for HPV antibodies. A cervicography is performed once in the first year and at 24 and 48 months. Considering the public health and economic importance of cervical cancer screening and given the current impetus within the federal government to examine the utility of HPV testing in augmenting existing screening programs, the investigators argue that there is a clear need for long-ranging multidisciplinary studies of the natural history of this malignant disease. In brief, this ongoing investigation will further understanding of the etiopathogenesis of cervical neoplasia by tackling the following specific objectives: (1) to study the prevalence and incidence of transient and persistent cervical HPV infection in asymptomatic women; (2) to verify the hypothesis that persistent HPV infection increases risk of low grade and high grade cervical lesions; (3) to search for epidemiologic determinants of persistent cervical HPV infection; (4) to search for specific molecular variants of oncogenic types of HPV that may be associated with an increased risk of cervical neoplasia; (5) to verify the hypothesis that measures of viral burden in the cervix may be correlated with persistent infections and with low and high grade lesions; and (6) to study the humoral immune response to capsid antigens of HPV as a possible marker of persistence of cervical HPV infection and of likelihood of progression in lesion severity.