Papillomavirus life cycle organization and biomarker selection.

Papillomavirus life cycle organization and biomarker selection.
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DOI:
10.1155/2007/613150
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发表时间:
2007
期刊:
影响因子:
--
通讯作者:
Doorbar J
Doorbar J
中科院分区:
医学4区
文献类型:
--
作者:
Doorbar J

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人乳头瘤病毒(HPV)是一组不同的病毒,可引起不同严重程度的上皮病变。在已经确定的100种左右的类型中,大约40种可以感染宫颈,其中一部分导致病变,这些病变可以进展为高级别肿瘤和宫颈癌。这些高风险类型在一般人群中普遍存在,并且可能使无法解决感染的妇女容易患癌症。病毒感染通常导致产生扁平疣,或使病毒基因组维持在无症状或潜伏状态。病毒合成依赖于病毒基因产物的有序表达,因为感染的基底细胞向上皮表面迁移。E7在较低的上皮层中表达,并且随后最终在更靠近上皮表面处表达E4和L1。这种有序模式在肿瘤进展和潜伏期期间以特征性方式变化,并且可以在病毒基因组整合到宿主细胞染色体中后不可逆地固定。我们对表达模式及其意义的理解开始解释疾病进展的性质,并为选择可用于预测疾病状态和预后结果的生物标志物提供了合理的基础。
Human papillomaviruses (HPVs) are a diverse group of viruses that cause epithelial lesions of varying severity. Of the 100 or so types that have been identified, around 40 can infect the cervix, with a subset of these causing lesions that can progress to high-grade neoplasia and cervical cancer. These high-risk types are prevalent in the general population, and can predispose to the development of cancer in women who cannot resolve their infection. Virus infection usually leads to the establishment of productive flat warts, or to maintenance of the viral genome in an asymptomatic or latent state. Virus synthesis depends on the ordered expression of viral gene products as the infected basal cell migrates towards the epithelial surface. E7 is expressed in the lower epithelial layers, and is followed eventually by the expression of E4 and L1 closer to the epithelial surface. This ordered pattern changes in characteristic ways during neoplastic progression and latency, and can be irreversibly fixed following integration of the viral genome into the host cell chromosome. Our understanding of expression patterns and their significance, is beginning to explain the nature of disease progression, and offers a rational basis for the selection of biomarkers that may be used to predict disease status and prognostic outcome.
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