Ferreira Ana Rita, Ramalho Ana Catarina, Marques Mariana, Ribeiro Daniela
Institute of Biomedicine-iBiMED & Department of Medical Sciences, University of Aveiro, 3810-198 Aveiro, Portugal.
Cancers (Basel). 2020 Mar 10;12(3):646. doi: 10.3390/cancers12030646.
Human papillomaviruses (HPV) are the causative agents of the most common sexually transmitted infection worldwide. While infection is generally asymptomatic and can be cleared by the host immune system, when persistence occurs, HPV can become a risk factor for malignant transformation. Progression to cancer is actually an unintended consequence of the complex HPV life cycle. Different antiviral defence mechanisms recognize HPV early in infection, leading to the activation of the innate immune response. However, the virus has evolved several specific strategies to efficiently evade the antiviral immune signalling. Here, we review and discuss the interplay between HPV and the host cell innate immunity. We further highlight the evasion strategies developed by different HPV to escape this cellular response and focus on the correlation with HPV-induced persistence and tumorigenesis.
人乳头瘤病毒（HPV）是全球最常见性传播感染的病原体。虽然感染通常无症状且可被宿主免疫系统清除，但当持续性感染发生时，HPV可成为恶性转化的危险因素。进展为癌症实际上是复杂HPV生命周期的意外后果。不同的抗病毒防御机制在感染早期识别HPV，导致先天免疫反应激活。然而，该病毒已进化出几种特定策略以有效逃避抗病毒免疫信号传导。在此，我们综述并讨论HPV与宿主细胞先天免疫之间的相互作用。我们进一步强调不同HPV为逃避这种细胞反应而制定的逃避策略，并关注与HPV诱导的持续性感染和肿瘤发生的相关性。
