Syrjänen K J
Pathol Annu. 1986;21 Pt 1:53-89.
Human papillomaviruses (HPV) consist of a heterogenic group of viruses (32 different HPV types currently recognized) known to induce a variety of squamous cell tumors (papillomas and warts) in the skin, and on mucous membranes of respiratory, gastrointestinal, and genitourinary tracts. The most familiar HPV manifestation in the genital tract is the venereal wart (condyloma acuminatum) recognized since antiquity, and shown to be a sexually transmitted disease (STD). In 1976, two other morphologically distinct HPV lesions were described in the uterine cervix, currently known as a flat and an inverted condyloma. Subsequently, these new HPV lesions were also shown to be an STD, and in addition, they frequently seem to occur concomitantly with CIN, CIS, and occasionally with invasive cervical carcinomas as well. These morphologic findings substantiated by the recent reports on malignant transformation of HPV lesions, as well as data from animal experiments and epidemiologic surveys, have lent support to the concept that HPV might be involved in the development of cervical (and other) human squamous cell carcinomas. Further evidence has been provided by the recent discoveries of HPV structural proteins (viral antigens) and HPV type 11 DNA in lesions of CIN, and HPV 16 and 18 DNA predominantly in invasive cervical carcinomas. So far, HPV 16 and HPV 18 seem to be the only HPV types with DNA capable of existing integrated in the host cell DNA. At the moment, cervical (and other) HPV lesions are the subject of intense study utilizing epidemiologic, morphologic, immunohistochemical, biochemical, and molecular biologic methods (recombinant gene technology) to provide further evidence of the suggested causal relationship between HPV and cancer. Prospective follow-up studies are also in progress to explore the natural history of cervical HPV lesions as well as the factors (e.g., immunologic, epidemiologic synergistic actions,) modifying them. In the light of present understanding, the factors linking HPV to cervical squamous cell carcinogenesis can be summarized as follows: (1) HPV infection in the uterine cervix is a sexually transmitted disease; (2) HPV lesions in the uterine cervix seem to be equivalent to CIN in their clinical behavior, i.e., possess the potential to progress towards CIS; (3) malignant transformation seems to depend on HPV type, being conditioned by integration of HPV DNA with the host cell DNA; (4) malignant transformation most probably requires synergistic effects between the virus and chemical or physical carcinogens, or other infectious agents; (5) genetic disposition (data available on animals only) significantly contributes to the process
人乳头瘤病毒（HPV）是一组异质性病毒（目前已识别出32种不同的HPV类型），已知可在皮肤以及呼吸道、胃肠道和泌尿生殖道的黏膜上诱发多种鳞状细胞瘤（乳头状瘤和疣）。生殖道中最常见的HPV表现是自古以来就已认识到的性病疣（尖锐湿疣），并已证实它是一种性传播疾病（STD）。1976年，在子宫颈中又描述了另外两种形态学上不同的HPV病变，目前称为扁平湿疣和内翻性湿疣。随后，这些新的HPV病变也被证明是一种性传播疾病，此外，它们似乎还经常与宫颈上皮内瘤变（CIN）、原位癌（CIS）同时出现，偶尔也与浸润性宫颈癌同时出现。最近关于HPV病变恶性转化的报道以及动物实验和流行病学调查的数据证实了这些形态学发现，支持了HPV可能参与宫颈（及其他）人类鳞状细胞癌发生发展的概念。CIN病变中HPV结构蛋白（病毒抗原）和HPV 11型DNA的最新发现，以及浸润性宫颈癌中主要为HPV 16和18型DNA的发现，提供了进一步的证据。到目前为止，HPV 16和HPV 18似乎是仅有的其DNA能够整合到宿主细胞DNA中的HPV类型。目前，宫颈（及其他）HPV病变正通过流行病学、形态学、免疫组织化学、生物化学和分子生物学方法（重组基因技术）进行深入研究，以进一步证明HPV与癌症之间可能存在因果关系。前瞻性随访研究也在进行中，以探索宫颈HPV病变的自然史以及影响它们的因素（如免疫、流行病学协同作用等）。根据目前的认识，将HPV与宫颈鳞状细胞癌发生联系起来的因素可总结如下：（1）子宫颈HPV感染是一种性传播疾病；（2）子宫颈HPV病变在临床行为上似乎与CIN相当，即具有发展为CIS的潜力；（3）恶性转化似乎取决于HPV类型，由HPV DNA与宿主细胞DNA的整合所决定；（4）恶性转化很可能需要病毒与化学或物理致癌物或其他感染因子之间的协同作用；（5）遗传易感性（仅在动物中有相关数据）对这一过程有显著影响
