Purtilo D T, Manolov G, Manolova Y, Harada S, Lipscomb H
IARC Sci Publ. 1984(63):749-70.
The immune system has evolved under Darwinian pressures as a defence against ubiquitous viruses. Immune surveillance against viral antigens protects the normal host. Individuals with inherited or acquired immune-deficiency disorders can become vulnerable to ubiquitous viruses and neoplasms can ensue, such as B-cell lymphoma, hepatocellular carcinoma, squamous-cell carcinoma, Kaposi's sarcoma, and carcinoma of the penis and uterine cervix. Immunodeficiency permits Epstein-Barr virus, hepatitis B virus, papillomavirus, herpes simplex virus, and cytomegalovirus to induce sustained target-cell proliferation. Each virus selects specific cellular targets bearing viral receptors and the infection leads to proliferation of the target cells rather than lysis. Various co-factors, including nutrition, exposure to tumour-promoting agents, parasitic infection, and ultraviolet light, may promote carcinogenesis. Depending on the type and severity of the immune deficiency, gradual proliferation may lead to evolution of a malignant clone. Conversion of polyclonal virally infected proliferating cells to give monoclonal malignancy is probably due to specific cytogenetic rearrangements which allow oncogene activation and endow an altered tumour cell with selective growth advantages over normal diploid cells. Prevention of viral oncogenesis may be possible by treatment of immune-deficient individuals with premalignant disorders. Immunotherapy and antiviral therapy may prevent progression of viral-induced proliferation to malignancy. The purpose of this paper is to discuss and evaluate the role of immune deficiency and viruses in the induction of malignancies commonly occurring in Africans residing in sub-Saharan Africa (Purtilo, 1976). The types of malignancies commonly occurring in this region are believed to be due to ubiquitous viruses. A failure of immune surveillance mechanisms to recognize viral antigens and abrogate proliferation of infected target cells predisposes to malignancy by increasing the chance of a proliferating cell undergoing a cytogenetic or molecular alteration which endows it with malignant characteristics. The immunological surveillance hypothesis has been elaborated during this century by Ehrlich, Thomas, Burnet, and Schwartz (reviewed by Purtilo & Linder, 1983). This hypothesis rests on several assumptions: that neoplastic cells possess unique tumour antigens: tumour antigens provoke an immune response in the host; and the immune response is protective and eliminates the tumour.(ABSTRACT TRUNCATED AT 400 WORDS)
在达尔文式的压力下，免疫系统不断进化，以抵御无处不在的病毒。针对病毒抗原的免疫监视保护着正常宿主。患有遗传性或获得性免疫缺陷疾病的个体可能会变得易受无处不在的病毒侵袭，继而引发肿瘤，如B细胞淋巴瘤、肝细胞癌、鳞状细胞癌、卡波西肉瘤以及阴茎癌和宫颈癌。免疫缺陷会使爱泼斯坦-巴尔病毒、乙型肝炎病毒、乳头瘤病毒、单纯疱疹病毒和巨细胞病毒诱导靶细胞持续增殖。每种病毒都会选择带有病毒受体的特定细胞靶点，感染会导致靶细胞增殖而非裂解。包括营养、接触促癌剂、寄生虫感染和紫外线在内的各种辅助因素可能会促进癌症发生。根据免疫缺陷的类型和严重程度，逐渐的增殖可能会导致恶性克隆的演变。多克隆病毒感染的增殖细胞转变为单克隆恶性肿瘤，可能是由于特定的细胞遗传重排，这种重排会激活癌基因，并赋予改变后的肿瘤细胞相对于正常二倍体细胞的选择性生长优势。通过治疗患有癌前疾病的免疫缺陷个体，有可能预防病毒致癌。免疫疗法和抗病毒疗法可能会阻止病毒诱导的增殖发展为恶性肿瘤。本文的目的是讨论和评估免疫缺陷和病毒在居住于撒哈拉以南非洲的非洲人常见恶性肿瘤诱发中的作用（Purtilo，1976）。该地区常见的恶性肿瘤类型被认为是由无处不在的病毒引起的。免疫监视机制未能识别病毒抗原并消除受感染靶细胞的增殖，通过增加增殖细胞发生细胞遗传或分子改变从而使其具有恶性特征的机会，易引发恶性肿瘤。免疫监视假说在本世纪由埃利希、托马斯、伯内特和施瓦茨进行了阐述（Purtilo和Linder综述，1983）。该假说基于几个假设：肿瘤细胞拥有独特的肿瘤抗原；肿瘤抗原在宿主体内引发免疫反应；并且免疫反应具有保护作用并能消除肿瘤。（摘要截选至400词）
