子宫颈癌(UCC)是全球最常见的妇科恶性肿瘤,近年来发病率不断上升。越来越多的证据表明,特定的病毒感染,包括人乳头瘤病毒(HPV),EB病毒(EBV)乙型肝炎和丙型肝炎病毒(HBV和HCV),和人类疱疹病毒(HHV),可能有助于UCC的发展和进步。了解病毒感染和UCC风险之间复杂的相互作用对于开发新的预防和治疗干预措施至关重要。
■本综述通过研究各种病毒病原体在UCC病因和发病机制中的作用,研究了病毒感染与UCC风险之间的关联。和可能的分子机制。此外,我们评估了针对病毒感染的UCC预防或治疗的现有诊断方法和潜在治疗策略.
■由于HPV检测作为重要工具的自我取样的出现,UCC的预防已大大推进,允许早期发现和干预。然而,UCC预防的一个基本挑战在于了解HPV和其他病毒共感染,包括EBV,HBV,HCV,HHV,艾滋病毒,或者它们同时存在,可能有助于UCC的发展。病毒感染与宫颈癌发展之间的关联的分子机制包括:(1)病毒癌基因与细胞调节蛋白的干扰,导致不受控制的细胞增殖和恶性转化;(2)病毒蛋白对肿瘤抑制基因的失活;(3)病毒逃避宿主免疫反应;(4)诱导持续的炎症反应,促进肿瘤微环境;(5)导致异常基因表达的表观遗传修饰;(6)病毒刺激血管生成;(7)病毒蛋白激活端粒酶,导致细胞永生化。此外,病毒共感染还可以通过病毒癌蛋白之间的协同相互作用增强致癌潜力,采用免疫逃避策略,导致慢性炎症,调节宿主细胞信号通路,并诱导表观遗传改变,最终导致宫颈癌的发生。
■认识到病毒癌基因在UCC病因和发病机制中的意义对于解决UCC不断升级的负担至关重要。开发创新的预防和治疗干预措施需要彻底了解病毒感染和UCC风险之间的复杂关系。
UNASSIGNED: Uterine Cervical Carcinoma (UCC) is the most prevalent gynecological malignancy globally, with a rising incidence in recent years. Accumulating evidence indicates that specific viral infections, including human papillomavirus (HPV), Epstein-Barr virus (EBV), Hepatitis B and C viruses (HBV and HCV), and human herpesvirus (HHV), may contribute to UCC development and progression. Understanding the complex interplay between viral infections and UCC risk is crucial for developing novel preventative and therapeutic interventions.
UNASSIGNED: This comprehensive review investigates the association between viral infections and UCC risk by examining the roles of various viral pathogens in UCC etiology and pathogenesis, and possible molecular mechanisms. Additionally, we evaluate current diagnostic methods and potential therapeutic strategies targeting viral infections for UCC prevention or treatment.
UNASSIGNED: The prevention of UCC has been significantly advanced by the emergence of self-sampling for HPV testing as a crucial tool, allowing for early detection and intervention. However, an essential challenge in UCC prevention lies in understanding how HPV and other viral coinfections, including EBV, HBV, HCV, HHV, HIV, or their concurrent presence, may potentially contribute to UCC development. The molecular mechanisms implicated in the association between viral infections and cervical cancer development include: (1) interference of viral oncogenes with cellular regulatory proteins, resulting in uncontrolled cell proliferation and malignant transformation; (2) inactivation of tumor suppressor genes by viral proteins; (3) evasion of host immune responses by viruses; (4) induction of a persistent inflammatory response, contributing to a tumor-promoting microenvironment; (5) epigenetic modifications that lead to aberrant gene expression; (6) stimulation of angiogenesis by viruses; and (7) activation of telomerase by viral proteins, leading to cellular immortalization. Additionally, viral coinfections can also enhance oncogenic potential through synergistic interactions between viral oncoproteins, employ immune evasion strategies, contribute to chronic inflammation, modulate host cellular signaling pathways, and induce epigenetic alterations, ultimately leading to cervical carcinogenesis.
UNASSIGNED: Recognizing the implications of viral oncogenes in UCC etiology and pathogenesis is vital for addressing the escalating burden of UCC. Developing innovative preventative and therapeutic interventions requires a thorough understanding of the intricate relationship between viral infections and UCC risk.