Feller L, Wood N H, Khammissa R A G, Chikte U M E, Meyerov R, Lemmer J
Department of Periodontology and Oral Medicine, School of Oral Health Sciences, University of Limpopo, Medunsa Campus, South Africa.
SADJ. 2010 Jul;65(6):266-8.
Host immune responses to HPV are generally low-level because the virus, being confined to basal epithelial cells is shielded from the circulating immune cells during initial stages of infection. In this location there is only a limited expression of viral proteins. Other factors contributing to the low level of host immunity are that HPV infection is non-lytic (does not cause death of the infected cell); that a functionally active immune response is generated only at later stages of HPV infection, in post-mitotic suprabasal keratinocytes where all viral genes are expressed; and that only in suprabasal keratinocytes has the HPV DNA been sufficiently amplified to be detected by the host immune-surveillance cells. In addition to the natural low-level immune responses towards HPV, HPV also employs several mechanisms to down-regulate innate and cell-mediated immunity, thus facilitating host immune evasion and persistent infection. The environment, lifestyle, the genetic make-up of the host, and the viral genomic characteristics can also influence the persistence of HPV infection, and consequential diseases. Persistent infection with high-risk HPV is associated with increased risk of developing HPV-mediated premalignancy and malignancy. It is not clear if the natural humoral immune response as opposed to vaccination is effective in eliminating primary HPV infection or in preventing progression of infection; but after initial infection, the host develops HPV-specific T cell immune responses that appear to be capable of clearing established infection, of protecting against progression of early HPV-associated intraepithelial neoplastic lesions to squamous cell carcinoma, and of preventing reinfection.
宿主对人乳头瘤病毒（HPV）的免疫反应通常处于低水平，因为在感染初期，该病毒局限于基底上皮细胞，从而免受循环免疫细胞的影响。在此位置，病毒蛋白的表达有限。导致宿主免疫水平低下的其他因素包括：HPV感染是非裂解性的（不会导致受感染细胞死亡）；只有在HPV感染后期，即在所有病毒基因都表达的有丝分裂后上层角质形成细胞中，才会产生功能活跃的免疫反应；并且只有在上层角质形成细胞中，HPV DNA才会充分扩增，从而被宿主免疫监视细胞检测到。除了对HPV的天然低水平免疫反应外，HPV还采用多种机制下调先天性免疫和细胞介导的免疫，从而促进宿主免疫逃逸和持续感染。环境、生活方式、宿主的基因构成以及病毒基因组特征也会影响HPV感染的持续性以及相关疾病。高危型HPV的持续感染会增加发生HPV介导的癌前病变和恶性肿瘤的风险。尚不清楚与疫苗接种不同的天然体液免疫反应是否能有效消除原发性HPV感染或预防感染进展；但在初次感染后，宿主会产生HPV特异性T细胞免疫反应，这些反应似乎能够清除已建立的感染，预防早期HPV相关上皮内肿瘤性病变进展为鳞状细胞癌，并防止再次感染。
