Hazra Rohan, Mackall Crystal
Pediatric Oncology Branch, National Cancer Institute, Bldg. 10-CRC Rm. 1W-3940, 10 Center Drive, MSC 1104, Bethesda, MD 20892, USA.
Curr HIV/AIDS Rep. 2005 Feb;2(1):24-8. doi: 10.1007/s11904-996-0005-2.
Current models hold that CD4+ depletion occurs as a result of direct and indirect effects of HIV, which both kill peripheral CD4+ cells and prevent adequate regeneration. Although age-associated involution diminishes thymic reserve and HIV is clearly thymotoxic, clinical trials have nonetheless shown that large proportions of patients who sustain adequate control of viral replication with highly active antiretroviral therapy (HAART) will demonstrate some evidence for thymic-dependent immune reconstitution, which is associated with improved immune competence. Furthermore, patients with insufficient or absent immune reconstitution following HAART generally lack evidence for thymopoiesis. Current studies are focused on improving our understanding of the causes for thymic failure in HIV infection. Recent work has demonstrated that some HIV strains, especially those that are CXCR4 trophic, are more thymotoxic and may contribute to irreversible thymic damage in this population.
目前的模型认为，CD4+细胞耗竭是由HIV的直接和间接作用导致的，HIV既能杀死外周血CD4+细胞，又能阻止其充分再生。尽管与年龄相关的退化会减少胸腺储备，且HIV显然具有胸腺毒性，但临床试验仍表明，很大一部分通过高效抗逆转录病毒疗法（HAART）实现病毒复制充分控制的患者会表现出一些胸腺依赖性免疫重建的证据，这与免疫能力的改善有关。此外，HAART后免疫重建不足或缺乏的患者通常缺乏胸腺生成的证据。目前的研究集中在增进我们对HIV感染中胸腺功能衰竭原因的理解。最近的研究表明，一些HIV毒株，尤其是那些亲嗜CXCR4的毒株，胸腺毒性更强，可能导致该人群中胸腺的不可逆损伤。
