Institute of Virology, Saarland University Medical Center, 66421 Homburg/Saar, Germany.
Viruses. 2017 Sep 12;9(9):254. doi: 10.3390/v9090254.
Human papillomavirus (HPV) infection is a causative factor for various cancers of the anogenital region and oropharynx, and is supposed to play an important cofactor role for skin carcinogenesis. Evasion from immunosurveillance favors viral persistence. However, there is evidence that the mere presence of oncogenic HPV is not sufficient for malignant progression and that additional tumor-promoting steps are required. Recent studies have demonstrated that HPV-transformed cells actively promote chronic stromal inflammation and conspire with cells in the local microenvironment to promote carcinogenesis. This review highlights the complex interplay between HPV-infected cells and the local immune microenvironment during oncogenic HPV infection, persistence, and malignant progression, and discusses new prospects for diagnosis and immunotherapy of HPV-associated cancers.
人乳头瘤病毒(HPV)感染是导致肛门生殖器区域和口咽各种癌症的一个致病因素,并且被认为在皮肤癌发生中起重要的协同作用因素。逃避免疫监视有利于病毒持续存在。然而,有证据表明,单纯存在致癌 HPV 不足以导致恶性进展,还需要其他促进肿瘤的步骤。最近的研究表明,HPV 转化细胞会积极促进慢性基质炎症,并与局部微环境中的细胞协同作用,促进癌变。这篇综述强调了致癌 HPV 感染、持续存在和恶性进展过程中 HPV 感染细胞与局部免疫微环境之间的复杂相互作用,并讨论了 HPV 相关癌症的新的诊断和免疫治疗前景。