IMMUNOBIOLOGY OF SIV ASSOCIATED LYMPHOMAS: CANCER

非霍奇金？S淋巴瘤发生频率增加(3-6%)。 感染艾滋病毒的人。这些艾滋病相关淋巴瘤(AAL) 表现出与淋巴瘤不同的特征 普通人口。急性淋巴细胞性白血病发病机制的新模型 包括1)肿瘤形成是多步骤的；2)肿瘤的发生 长期存活者；3)肿瘤来源于克隆性B细胞；4)HIV 起作用早，是间接效应者；5)肿瘤细胞被感染 EBV；6)特定的遗传损伤发生在肿瘤细胞中。许多 这一过程的各个方面仍需在动物模型系统中进行测试。 自1984年以来，对感染SIV的恒河猴和食蟹猴进行了1200多例尸检 猴子已经在TRPRC表演过。淋巴系统恶性肿瘤 在一定比例的SIV感染动物中检测到。这些 SAID相关淋巴瘤(SAL)已被组织学研究， 免疫组织化学、原位杂交、Southern印迹和 聚合酶链式反应以确定其病理特征的程度 概述AAL发病机制的工作模型。结果是 显示淋巴瘤发生在感染SIV的恒河猴身上 AAL的发病率与AAL相似，而SAL的发病率在 食蟹猴的体重要高出8倍。从两个方面分析SAL 猕猴的物种表现出与 急性淋巴细胞性白血病的病理生物学特征。肿瘤发生在 SAID的长期幸存者，表现出结外解剖 分布，代表B细胞起源的克隆性扩增，缺乏SIV 在肿瘤细胞中，并感染RhLCV(一种密切相关的疱疹病毒 与EBV有关)。这些发现表明，感染艾滋病毒的人 感染SIV的猕猴具有共同的病理生物学和发病机制 淋巴增生症的症状。为NIH-NCI RO1 CA74731提供资金(征税，PI) 出版物：Baskin GB，A Habis，M Murphey-Corb，LS Levy。 恒河猴SIV相关淋巴瘤--艾滋病相关模型 淋巴瘤。第16届非人学术年会论文集 艾滋病的灵长类动物模型，佐治亚州亚特兰大，(第41号摘要)，1998。

Non-Hodgkin?s lymphomas occur with increased frequency (3-6%) in HIV-infected individuals. These AIDS-associated lymphomas (AAL) exhibit characteristics that distinguish them from lymphomas in the general population. A proposed model for the pathogenesis of AAL includes the following 1) Tumorigenesis is multistep; 2) Tumors occur in long-term survivors; 3) Tumors are of clonal B-cell origin; 4) HIV acts early and is an indirect effector; 5) tumor cells are infected with EBV; and 6) Specific genetic lesions occur in tumor cells. Many aspects of this process remain to be tested in an animal model system. Since 1984, over 1200 necropsies on SIV-infected rhesus and cynomolgus monkeys have been performed at the TRPRC. Lymphoid malignancies were detected in a proportion of SIV-infected animals. These SAIDS-associated lymphomas (SAL) have been studied by histology, immunohistochemistry, in situ hybridization, Southern blotting, and PCR to determine the extent to which their pathologic al features recapitulate a working model for the pathogenesis of AAL. The results show that lymphomas occur in SIV-infected rhesus macaques at an incidence similar to that of AAL, and that the incidence of SAL in cynomolgus macaques is 8-fold higher. Analysis of SAL from both species of macaques demonstrated significant similarity to the hallmark pathobiological features of AAL. The tumors occur in long-term survivors of SAIDS, exhibit extranodal anatomic distribution, represent clonal expansions of B-cell origin, lack SIV in tumor cells, and are infected with RhLCV (a herpesvirus closely related to EBV). These findings indicate that the HIV-infected human and the SIV-infected macaque share a common pathobiology and mechanism of lymphomagenesis. FUNDING NIH-NCI RO1 CA74731 (Levy, PI) PUBLICATIONS Baskin GB, A Habis, M Murphey-Corb, LS Levy. SIV-associated lymphoma in rhesus monkeys a model for AIDS-associated lymphoma. Proceedings of the 16th Annual Symposium on Nonhuman Primate Models for AIDS, Atlanta, GA, (Abstract # 41), 1998.