Pathogenic Mechanisms In HIV Disease

研究表明，间歇性输注T细胞衍生的细胞因子IL-2可导致CD 4+池的大小显著增加。对IL-7/IL-7受体（CD 127）系统的分析显示，尽管进行了抗逆转录病毒或IL-2治疗，但HIV感染患者T细胞上的CD 127表达较低，并且仍然较低，反映了T细胞库亚群组成的持续畸变。在另一项研究中，与先前的报告相反，蠕虫感染的治疗并没有导致艾滋病毒复制水平的降低，这表明艾滋病毒感染免疫激活和继发感染之间的关系具有复杂的性质。 在其他工作中，在对HIV蛋白酶抑制剂具有高水平抗性的患者中注意到一系列新的突变。这些突变涉及结合位点、切割位点和控制总体复制能力的区域的变化。最后，发现放线菌素D增加HIV复制的矛盾能力是由于IL-6的诱导。

Studies have demonstrated that intermittent infusions of the T cell derived cytokine IL-2 can lead to profound increases in the size of the CD4+ pool. An analysis of the IL-7/IL-7 receptor (CD127) system revealed that CD127 expression on T cells was low and remained low in HIV-infected patients despite antiretroviral or IL-2 therapy, reflecting persistent aberration in the subset composition of the T-cell pool. In another study, contrary to prior reports, treatment of helminthic infection did not lead to a decrease in levels of HIV replication indicating the complex nature of the relationships between HIV infection immune activation and secondary infections. In other work, a novel series of mutations were noted in a patient with high-level resistance to HIV protease inhibitors. These mutations involved changes in the binding site, the cleavage site and in areas controlling overall replication competence. Finally, the paradoxical ability of Actinomycin D to increase HIV replication was found to be due to the induction of IL-6.