摘要
目的观察杀伤性细胞免疫球蛋白样受体3DS1（KIR3DS1）及Bw4^80IIe是否影响急性HIV-1患者的病毒调定点水平和CD4细胞计数。方法用特异性引物-聚合酶链反应（SSP—PCR）技术检测2006-2012年北京佑安医院109例急性HIV-1患者KIR3DL1、KIR3DS1基因型、人白细胞抗原（HLA）-B分子Bw4、Bw6分型；测序分析Bw4第80位氨基酸的分类（Bw4^80IIe和Bw4^80Thr）。结果（1）携带KIR3DL1／KIR3DL1、KIR3DS1／KIR3DS1和KIR3DL1／KIR3DS1的急性HIV-1患者病毒调定点分别是4．35±0．79、4．24±0．49和3．99±0．85。KIR3DL1／KIR3DS1患者的病毒调定点显著低于KIR3DL1／KIR3DL1患者（P=0．032）。（2）携带Bw4^80IIe、Bw4^80Thr和Bw6／6的患者病毒调定点分别是3．89±0．49、4．20±1．03、4．44±0．59，单因素方差分析显示差异有统计学意义（P=0．027），且Bw4^80IIe患者的病毒调定点显著低于Bw6／6患者（P=0．020）。（3）携带KIR3DS1和Bw4^80IIe的HIV-1患者病毒调定点为3．26±0．81，低于其他组患者（均P〈0．05）。携带KIR3DS1和Bw4^80IIe的患者中只有较少患者在HIV-1感染后3年内CIM细胞计数下降到350个／μl以下，尤其与携带KIR3DS1和Bw6／6（P=0．006）、KIR3DL1和Bw6／6（P=0．015）、KIR3DL1和Bw4^80IIe（P=0．0196）的患者比较更少。结论Bw4^80IIe在KIR3DS1存在时与病毒调定点低有关，延迟了HIV-1患者CD4细胞计数下降。
Objective To investigate whether killer cell immunoglobulin-like receptor 3DS1 （KIR3DS1） and Bw4^80IIe could play a protective role during HIV-1 infection. Methods KIR3DL1/3DS1 and Bw4, Bw6 were genotyped by SSP-PCR and Bw4 allotypes （Bw4^80IIe and Bw4^80Thr） were classified via sequencing among 109 individuals acutely infected with HIV-1 in Beijing You＇an Hospital between 2006 and 2012. Results （ 1 ） Of the 109 patients, 65,7, and 37 subjects respectively harbored KIR3DL1/KIR3DL1, KIR3DS1/KIR3DS1, and KIR3DL1/KIR3DS1 genotypes. Their viral set points were determined as 4. 35 ± 0. 79,4. 24 ± 0. 49 and 3.99 ± 0. 85 respectively. The viral set point of patients carrying KIR3DL1/KIR3DS1 was significantly lower than the KIR3DL1/KIR3DL1 genotype patients （P = 0. 032）. （2）26,41,42 subjects harbored Bw4^80IIe, Bw4^80Thrs, Bw6/6, respectively. Viral set points of these subjects were respectively 3.89 ± 0. 49,4. 20± 1.03 and 4.44 ±0. 59. One-way ANOVA indicated that Bw4S^80IIe influenced the levels of viral set point （P = 0. 027 ）. Moreover, the level of viral set point of the Bw4^80IIe genotype was significantly lower than the Bw6/6 genotype （P = 0. 020）. These outcomes indicated Bw4^80IIe was associated with lower levels of viral set point. （3）Viral set point of patients harboring KIR3DS1 and Bw4^80IIe was 3.26 ± 0. 81 and significantly lower than individuals possessing other genotypes （all P 〈 0.05 ）. KIR3DS1 and Bw4^80IIe conferred an advantage over other genotypes, especially over KIR3DS1 and Bw6/6 （P = 0. 006 ） , K1R3DL1 and Bw6/6 （P = 0. 015） and even KIR3DL1 and Bw4^80IIe （P = 0. 019 6） in delaying CD4 count decline within 3 years after HIV-1 infection. Conclusions KIR3DS1 and Bw4^80IIe are synergistically related to lower viral set point and slowing down the CD4 count decline as Bw4^80IIe in the presence of KIR3DS1.
作者
王蕊
刘妍
陆小凡
刘志英
李珍
张欣
Wang Rui;Liu Yan;La Xiaofan;Liu Zhiying;Li Zhen;Zhang Xin(Beijing Key Laboratory for HIV/AIDS Research,Center for Infectious Diseases,Beijing You＇an Hospital,Capital Medical University,Belting 100054,China)
出处
《中华医学杂志》
CAS
CSCD
北大核心
2018年第35期2819-2823,共5页
National Medical Journal of China
基金
国家自然科学基金（81501731,81501732,81772165,81571973）
艾滋病研究北京市重点实验室（BZ0089）
