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Host control of human papillomavirus infection and disease

机译:宿主控制人乳头瘤病毒感染和疾病

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Most human papillomaviruses cause inapparent infections, subtly affecting epithelial homeostasis, to ensure genome persistence in the epithelial basal layer. As with conspicuous papillomas, these self-limiting lesions shed viral particles to ensure population level maintenance and depend on a balance between viral gene expression, immune cell stimulation and immune surveillance for persistence. The complex immune evasion strategies, characteristic of high-risk HPV types, also allow the deregulated viral gene expression that underlies neoplasia. Neoplasia occurs at particular epithelial sites where vulnerable cells such as the reserve or cuboidal cells of the cervical transformation zone are found. Beta papillomavirus infection can also predispose an individual with immune deficiencies to the development of cancers. The host control of HPV infections thus involves local interactions between keratinocytes and the adaptive immune response. Effective immune detection and surveillance limits overt disease, leading to HPV persistence as productive microlesions or in a true latent state. (C) 2017 Published by Elsevier Ltd.
机译:大多数人乳头瘤病毒导致不公平的感染,巧妙地影响上皮性稳态,以确保上皮基底层的基因组持续存在。与显着的乳头瘤一样,这些自限损伤脱落病毒颗粒以确保人口水平维持,并取决于病毒基因表达,免疫细胞刺激和免疫监测的平衡。复杂的免疫逃号策略,高风险HPV类型的特征,也允许解毒的病毒基因表达,使瘤形成下面。肿瘤发生在特定的上皮部位,其中发现诸如宫颈转化区的储备或立方体细胞的脆弱细胞。 βPapillomaVirus感染还可以使个体易受免疫缺陷的癌症的发育。因此,HPV感染的宿主控制涉及角质形成细胞与适应性免疫应答之间的局部相互作用。有效的免疫检测和监测限制公开疾病,导致HPV持久性作为生产性微调或真正的潜在状态。 (c)2017年由elestvier有限公司出版

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