International Centre for Genetic Engineering and Biotechnology, Trieste, Italy.
APMIS. 2010 Jun;118(6-7):471-93. doi: 10.1111/j.1600-0463.2010.02618.x.
Persistent infection by a subgroup of so-called high-risk human papillomaviruses (HPVs) that have a tropism for mucosal epithelia has been defined as the cause of more than 98% of cervical carcinomas as well as a high proportion of other cancers of the anogenital region. Infection of squamous epithelial tissues in the head and neck region by these same high-risk HPVs is also associated with a subset of cancers. Despite the general conservation of genetic structure amongst all HPV types, infection by the low-risk types, whether in genital or head and neck sites, carries a negligible risk of malignant progression, and infections have a markedly different pathology. In this review, we will examine and discuss the interactions that the principal viral oncoproteins of the high-risk mucosotrophic HPVs and their counterparts from the low-risk group make with cellular target proteins, with a view to explaining the differences in their respective pathology.
持续感染所谓的高危型人乳头瘤病毒(HPV),这些 HPV 具有黏膜上皮的趋向性,已被定义为超过 98%的宫颈癌以及相当一部分其他肛门生殖器区域癌症的病因。这些相同的高危型 HPV 也会感染头颈部的鳞状上皮组织,与某些癌症有关。尽管所有 HPV 类型在遗传结构上普遍保持一致,但低危型 HPV 的感染,无论是在生殖器还是头颈部,恶性进展的风险可忽略不计,且感染具有明显不同的病理学。在这篇综述中,我们将研究和讨论高危黏膜嗜性 HPV 的主要病毒致癌蛋白及其来自低危型组的对应物与细胞靶蛋白的相互作用,以期解释它们各自病理学的差异。