Castro-Muñoz Leonardo Josué, Rocha-Zavaleta Leticia, Lizano Marcela, Ramírez-Alcántara Katia Montserrat, Madrid-Marina Vicente, Manzo-Merino Joaquín
The Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA.
Unidad de Investigación Biomédica en Cáncer, Instituto Nacional de Cancerología, México/Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Av. San Fernando No. 22, Col. Sección XVI, Tlalpan, Mexico City 14080, Mexico.
Biomedicines. 2022 Nov 17;10(11):2965. doi: 10.3390/biomedicines10112965.
A persistent infection with the so-called high-risk Human Papillomaviruses (hr-HPVs) plays a fundamental role in the development of different neoplasms. The expression of the HPV proteins throughout the different steps of the viral life cycle produce a disruption of several cellular processes, including immune response, which can lead to cell transformation. The interferon-mediated response plays an important role in eliminating HPV-infected and -transformed cells. The ability of HPV to disrupt the proper function of the interferon response is based on a series of molecular mechanisms coordinated by HPV proteins intended to prevent clearance of infection, ultimately producing an immunotolerant environment that facilitates the establishment of persistence and cancer. In this review, we focus on the molecular actions performed by HPV E1, E2, E5, E6 and E7 proteins on IFN signaling elements and their contribution to the establishment of infection, viral persistence and the progression to cancer.
感染所谓的高危型人乳头瘤病毒(hr-HPVs)持续存在在不同肿瘤的发生发展中起重要作用。HPV蛋白在病毒生命周期的不同阶段表达,会破坏包括免疫反应在内的多个细胞过程,从而导致细胞转化。干扰素介导的反应在清除HPV感染和转化的细胞中起重要作用。HPV破坏干扰素反应正常功能的能力基于一系列由HPV蛋白协调的分子机制,旨在防止感染被清除,最终产生一个免疫耐受环境,有利于持续性感染和癌症的发生。在这篇综述中,我们重点关注HPV E1、E2、E5、E6和E7蛋白对IFN信号元件的分子作用,以及它们在感染建立、病毒持续性和癌症进展中的作用。