HPV replicative cycle and role of viral proteins in lesion progression

Concilium Pub Date : 2024-04-03 DOI:10.53660/clm-3180-24f33
Ximenya Glauce da Cunha Freire Lopes, Jenner Chrystian Veríssimo de Azevedo, Amanda Estevam Carvalho, V. D. D. Almeida, J. Araújo, V. S. Andrade, R. Cobucci, Christiane Medeiros Bezerra, T. A. A. Fernandes, José Veríssimo Fernandes
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Abstract

Human papillomaviruses are DNA viruses that primarily infect the stratified squamous epithelium of the genital tract mucosa. Some of these viruses are strongly associated with cervical cancer. They are sexually transmitted agents that are highly prevalent around the world. Most infections heal spontaneously, in approximately 18 to 24 months, but in some individuals, the virus persists in a latent, asymptomatic form or a productive form, causing cervical intraepithelial lesions that may progress to result in invasive cervical cancer. During productive infection, the virus executes a complex interaction program with the host cell dependent on differentiation and, through its proteins, nullifies the host cell's protective mechanisms against malignant transformation and suppresses the host's immune responses. Initial lesions may spontaneously revert, but those that reach a certain stage, if not treated, progress to malignant forms. In this review, we present some advances in the biology of HPV infection and the role of its proteins in the interaction with the host cell and its consequences.
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HPV 复制周期和病毒蛋白在病变进展中的作用
人类乳头瘤病毒是 DNA 病毒,主要感染生殖道粘膜的分层鳞状上皮。其中一些病毒与宫颈癌密切相关。它们是性传播的病原体,在世界各地都非常普遍。大多数感染会在大约 18 至 24 个月内自愈,但在某些人身上,病毒会以潜伏、无症状或产生性感染的形式持续存在,导致宫颈上皮内病变,并可能发展为浸润性宫颈癌。在生产性感染期间,病毒会与宿主细胞进行复杂的相互作用,这种相互作用依赖于分化,并通过其蛋白质使宿主细胞防止恶性转化的保护机制失效,并抑制宿主的免疫反应。最初的病变可能会自发恢复,但达到一定阶段的病变如果得不到治疗,就会发展为恶性病变。在这篇综述中,我们将介绍 HPV 感染生物学方面的一些进展,以及 HPV 蛋白在与宿主细胞相互作用中的作用及其后果。
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