Prevalence of HPV in the Oral Cavity of HIV+ Individuals

描述（由申请人提供）：人类免疫缺陷病毒（HIV）已感染全球超过3300万人，导致CD4+ T细胞选择性耗竭导致免疫抑制。 这种免疫力的缺乏导致许多机会性感染，其中超过50%的HIV感染个体发展出涉及口腔的病理学。 导致HIV+患者口腔疾病的病原体之一是粘膜萎缩性人乳头瘤病毒（HPV）。 虽然HPV不能常规培养，但它是最常见的病毒性性传播疾病。 HPV是口腔和生殖器疣、局灶性上皮增生以及大部分宫颈癌、肛门生殖器癌和口腔鳞状细胞癌的病原体。 HIV合并感染导致HPV生殖器感染率增加，HPV持续性增加，HPV相关病变（宫颈或肛门发育不良）的发生率增加，这更难治疗。同样，初步研究表明，HIV合并感染导致口腔HPV和HPV相关口腔病变（包括口腔癌）的患病率增加。 令人惊讶的是，用高效抗逆转录病毒疗法（HAART）治疗HIV导致明显的HPV相关口腔疣增加。 这些疣大，疼痛，难以治疗。继续使用HAART的HIV+患者可能会导致口腔疣和其他HPV相关的口腔病理，如鳞状细胞癌的发病率大幅增加。 迄今为止的研究受到用于检测HPV感染的分子技术的缺乏或限制范围的限制。 因此，对口腔HPV感染的患病率、感染部位和自然史知之甚少。 更好地了解口腔HPV感染，特别是在HIV+合并感染的个体中，对于预防HPV相关的口腔病理学至关重要。 初步数据表明，利用为检测生殖器HPV而开发的共有PCR引物组检测口腔HPV感染的能力。 这些技术可以扩展到检测口腔HPV类型。 我们假设，可以开发一种基于PCR的高通量口腔HPV类型检测方法，并用于确定HIV+个体队列中口腔HPV感染的患病率和部位

DESCRIPTION (provided by applicant): Human immunodeficiency virus (HIV) has infected over 33 million people worldwide leading to immune suppression from the selective depletion of CD4+ T cells. This lack of immunity results in numerous opportunistic infections with over 50% of the HIV-infected individuals developing pathology involving the oral cavity. Among the pathogens responsible for oral disease in HIV+ patients is the mucosatropic human papillomavirus (HPV). Although HPV cannot be routinely cultured, it is the most common viral sexually transmitted disease. HPV is the etiologic agent of oral and genital warts, focal epithelial hyperplasia, and a large proportion of cervical, anogenital, and oral squamous cell carcinomas. HIV co-infection leads to increased rate of HPV genital infection, increased HPV persistence, and increased rates of HPV-related pathology (cervical or anal dysplasia), which is more difficult to treat. Similarly, preliminary studies indicate that HIV co-infection leads to increases in the prevalence of oral HPV and HPV-related oral pathology including oral cancer. Surprisingly, treatment of HIV with highly active anti-retroviral therapy (HAART) has led to increases in apparent HPV-related oral warts. These warts have been large, painful, and difficult to treat. Continued use of HAART for the HIV+ patient may lead to substantial increases in the incidence of oral warts and other HPV-related oral pathology such as squamous cell carcinomas. The studies to date have been limited by the lack of or the restrictive scope of the molecular techniques used to detect HPV infection. Thus, little is known about the prevalence, site of infection and natural history of oral HPV infection. A better understanding of oral HPV infection particularly in the HIV+ co-infected individual is of paramount importance in order to prevent HPV-related oral pathology. Preliminary data demonstrates the ability to detect oral HPV infection utilizing consensus PCR primer sets that were developed for detection of genital HPV. These techniques can be extended to detect oral HPV types. We hypothesize that a high throughput PCR-based method for detecting oral HPV types can be developed and utilized to determine the prevalence and site of oral HPV infection in a cohort of HIV+ individuals