提高胸腺功能、促进免疫重建是艾滋病治疗的重要策略。虽然该领域已有IL-7、IL-15等多种有潜力的药物正在研制，但尚无成熟方案。HNA-1为课题组专利中药，临床应用十年来疗效满意；前期在小鼠免疫缺陷模型和猴艾滋病模型上均证实该药能显著提高初始型CD4+T细胞水平，且已初步证明其可促进CD34+细胞归巢到胸腺、促进胸腺细胞分化及提高胸腺输出，提示其机制与调节胸腺基质细胞的视黄酸诱导基因蛋白I样受体（RLR）/线粒体抗病毒信号蛋白（MAVS）通路有关。本项目拟从RLR/MAVS信号通路探讨HNA-1对HAART治疗慢性SIV感染免疫重建的促进作用、对急性SIV感染胸腺退化的调节作用和对poly(I:C)诱导的成年及老年小鼠胸腺退化的保护作用。研究结果将首次从RLR/MAVS信号通路介导胸腺细胞发育调节的角度阐明HNA-1的疗效机制，为艾滋病中药研发提供重要的实验依据。

Improving the thymopoiesis and immune reconstitution is an important complementary therapy for HIV-1 infection. Although IL-7, IL-15 and some other potential agents are in development, none of them has been validated by clinical trial. HNA-1, a Chinese herb preparation owned patent by the research group, has exhibited clinical effect in past ten years. We also evaluated its effect on cyclosporine A induced immunodeficiency in mouse and simian immunodeficiency virus infection in reshus monkeys. With both models, it increased the naïve CD4 significantly. Thereafter, we proved that HNA-1 was capable of augmenting the homing of CD34+ progenitor cell to thymus, prompting the development of thymocytes and increasing the thymic output through uncertain mechanisms, which is probably mediated by retinoic acid-inducible gene I (RIG-I) like receptors and mitochondrial antiviral signaling protein (MAVS) contributed signal pathway. In this study, we aimed to investigate the effects of HNA-1 on immune reconstitution of chronical SIV infected monkeys under HAART treatment, on thymus atrophy caused by acute SIV infection, and on thymus atrophy induced by poly(I:C)in adult and aged mice. The role of “RLR—MAVS” signal pathway in HNA-1’s protective effect will also be explored simultaneously. This study will extend our knowledge on the regulation of thymocytes developmen, reveal the underlying mechanisms of HNA-1 clinical effect, and prompt the development of agents targeting thymopoiesis and CD4 reconstitution.