Mohammed Mohammed Mohsen, Al-Khafaji Zaytoon Abdulrida Ighewish, Al-Hilli Nadia Mudher
Department of Microbiology, College of Medicine, University of Babylon, Hilla, Iraq.
Department of Obstetrics and Gynecology, College of Medicine, University of Babylon, Hilla, Iraq.
Tzu Chi Med J. 2024 Dec 3;37(1):28-41. doi: 10.4103/tcmj.tcmj_134_24. eCollection 2025 Jan-Mar.
The most common STD that triggers cervical cancer is the human papillomavirus. More than 20 types of human papillomavirus (HPV) can induce uterine cervical cancer. Almost all women acquire genital HPV infection soon after their first intercourse, with most of them clearing the virus within 3 years. An immune response is necessary to clear. The first responders to HPV infection are the innate immune system elements composed of macrophages, keratinocytes, natural killer cells, and natural killer T-lymphocytic (NKT) cells. Cytotoxic T lymphocytes (CTLs) comprise the second line of defense and kill HPV16-infected cells expressing various peptides derived from their transforming early viral oncoproteins, mainly E2•E6. Even though HPV can manage to trick away our immune systems, first of all, it is important to emphasize that HPV replication does not kill the host cells. It does not replicate viral antigens or cause inflammation. The HPV16 E6 and E7 genes suppress host cell type 1 interferons (IFNs), which are detectable after infection. The patient may have immunological tolerance; hence, there are no costimulatory signals from inflammatory cytokines like IFNs during antigen recognition. Evidence shows that HlA class I generations have been inhibited by HPV16 E5, which could protect this tumor cell from CTL attack. HPV16 E7 is responsible for initiating immunotolerance and increasing regulatory T cells (Treg) to repress immunological regression. Evasion from immune system protection plays a critical role in the outcome of persistent HPV infection and the development of cervical cancer. Vaccination against HPV16 and 18 during adolescence is the most effective method for preventing cervical cancer in women, considering the immunological processes involved.
引发宫颈癌最常见的性传播疾病是人类乳头瘤病毒。20多种人类乳头瘤病毒（HPV）可诱发子宫颈癌。几乎所有女性在首次性交后不久就会感染生殖器HPV，其中大多数人会在3年内清除病毒。清除病毒需要免疫反应。HPV感染的首批应答者是由巨噬细胞、角质形成细胞、自然杀伤细胞和自然杀伤性T淋巴细胞（NKT细胞）组成的先天免疫系统元件。细胞毒性T淋巴细胞（CTL）构成第二道防线，可杀死表达源自其转化早期病毒癌蛋白（主要是E2•E6）的各种肽的HPV16感染细胞。尽管HPV能够设法骗过我们的免疫系统，但首先需要强调的是，HPV复制不会杀死宿主细胞。它不会复制病毒抗原或引发炎症。HPV16 E6和E7基因会抑制宿主细胞1型干扰素（IFN），感染后可检测到这种干扰素。患者可能具有免疫耐受性；因此，在抗原识别过程中，不存在来自IFN等炎性细胞因子的共刺激信号。有证据表明，HPV16 E5抑制了HlA I类分子的产生，这可以保护这种肿瘤细胞免受CTL攻击。HPV16 E7负责引发免疫耐受性并增加调节性T细胞（Treg）以抑制免疫消退。逃避免疫系统保护在持续性HPV感染的结果和宫颈癌的发展中起着关键作用。考虑到所涉及的免疫过程，青春期接种针对HPV16和18的疫苗是预防女性宫颈癌最有效的方法。
