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AIDS 病一个显著特征是CD_4~+T 细胞功能障碍甚至被选择性清除,其原因至少有一部分是HIV-1与CD_4结合并感染CD_4~+T 细胞所致。因而,将抗病毒药物特异引向靶细胞(CD_4~+),能防止感染并抑制CD_4~+细胞前病毒DNA 产生HIV,从而具有治疗效应。已知美洲商陆抗病毒蛋白(PAP)可以抑制正常CD_4~+T 细胞内HIV-1复制。PAP 分子量约30KD,其功能是抑制一些植物病毒(RNAV)、单纯疱疹、脊髓灰质炎和流感病毒的增殖。作者报告将单抗T101(抗CD_5)、G3.7(CD_7)、B43(CD_(10))、G17-2(CD_1)分别与PAP 偶联成复合物,如此使PAP 杀细胞活性提高1000倍。由于导向PAP 只与3%的CD_4~+细胞作用,对于CD_4依赖性免疫应答影响不大。研究表明PAP 作用
A significant feature of AIDS is that CD_4 ~ + T cell dysfunction is even selectively eliminated, at least in part due to the binding of HIV-1 to CD_4 and the infection of CD_4 ~ + T cells. Therefore, the specific antiviral drug-directed target cells (CD_4 ~ +), to prevent infection and inhibit CD_4 ~ + pre-virus DNA to produce HIV, which has a therapeutic effect. Pokeweed antiviral protein (PAP) is known to inhibit HIV-1 replication in normal CD4 + T cells. PAP molecular weight of about 30KD, its function is to inhibit the proliferation of some plant viruses (RNAV), herpes simplex, poliomyelitis and influenza virus. The authors report the conjugation of mAbs T101 (anti-CD_5), G3.7 (CD_7), B43 (CD_ (10)) and G17-2 (CD_1) to PAP complexes, respectively, . As directed PAP only interacts with 3% of CD4 + cells, it has little effect on CD4-dependent immune responses. Research shows that PAP effect