IMMUNOBIOLOGY OF SIV ASSOCIATED LYMPHOMAS: CANCER

非霍奇金淋巴瘤S淋巴瘤的发生频率增加（3-6%）， 艾滋病毒感染者。 艾滋病相关淋巴瘤（AAL） 表现出区别于淋巴瘤的特征， 一般人口。 AAL发病机制的拟议模型 包括以下内容：1）肿瘤发生是多步骤的; 2）肿瘤发生 在长期存活者中; 3）肿瘤是克隆B细胞来源的; 4）HIV 早期作用，是间接效应器; 5）肿瘤细胞被感染 与EBV;和6）在肿瘤细胞中发生特异性遗传病变。 许多 该过程的各个方面仍有待在动物模型系统中进行测试。 自1984年以来，超过1200例SIV感染恒河猴和食蟹猴的尸检 在TRPRC对猴子进行了实验。 恶性淋巴瘤是 在SIV感染的动物中检测到。 这些 SAIDS相关淋巴瘤（SAL）已经通过组织学进行了研究， 免疫组织化学、原位杂交、Southern印迹和 PCR检测其病理学特征 概括了AAL发病机制的工作模型。 结果 表明淋巴瘤发生在SIV感染的恒河猴中， 发生率与AAL相似， 食蟹猴的死亡率高出8倍。 两者的SAL分析 种猕猴表现出显着的相似性， AAL的标志性病理生物学特征。 肿瘤发生在 SAIDS的长期存活者，表现出结节性解剖 分布，代表B细胞来源的克隆扩增，缺乏SIV 在肿瘤细胞中，并感染RhLCV（一种疱疹病毒， 与EBV有关）。 这些发现表明，艾滋病毒感染者 和SIV感染的猕猴有着共同的病理学和机制 淋巴瘤 资助NIH-NCI RO 1 CA 74731（Levy，PI） 出版物巴斯金GB，A Habis，M Murphey-Corb，LS Levy. 恒河猴SIV相关性淋巴瘤是艾滋病相关性淋巴瘤的模型 淋巴瘤 第16届非人类科学年会论文集 艾滋病的灵长类模型，亚特兰大，GA，（摘要#41），1998年。

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.