清除HIV潜伏的两种新方法

　　生物通报道，顽疾艾滋病一直为人们所头疼，抗艾滋病治疗的效果一直不理想，原因在于病毒隐匿在免疫细胞里，让抗逆转录病毒无计可施。目前，科学家们找到两种治疗隐匿HIV的方法。

　　

生物通报道，顽疾艾滋病一直为人们所头疼，抗艾滋病治疗的效果一直不理想，原因在于病毒隐匿在免疫细胞里，让抗逆转录病毒无计可施。目前，科学家们找到两种治疗隐匿HIV的方法。

 

加拿大和美国的科研人员开发出一种针藏身CD4细胞中的HIV的方法采用定向化疗，同时与定向免疫疗法结合，杀死藏身免疫细胞中的HIV，同时为免疫系统留出时间再生健康细胞。相关成果公布在最近一期的《Nature Medicine》上。

 

此外，美国加州大学和Gladstone研究所的科研人员在最近的一期《PLoS Pathogens》上发表类似的研究进展。

 

Eric Verdin发现，受感染细胞的DNA胞嘧啶甲基化与HIV潜伏相关，DNA甲基化促进潜伏的HIV再度活跃。导致治疗失效。

 

同时研究人员发现methlyl-CpG 结合域蛋白2（MBD2，methlyl-CpG binding domain protein 2）与甲基化的 HIV DNA 结合，进一步促进HIV活跃。

 

研究人员发现5-aza-2'deoxycytidine （aza-CdR，5-氮-2'-去氧胞嘧啶核苷）这种药物能抑制 HIV 甲基化，阻止HIV再度活跃。

 

这些研究成果为艾滋病治疗提供了全新的视野。

（生物通 小茜）

生物通推荐原文检索：Epigenetic Regulation of HIV-1 Latency by Cytosine Methylation

【Abstract】

Human immunodeficiency virus type 1 (HIV-1) persists in a latent state within resting CD4+ T cells of infected persons treated with highly active antiretroviral therapy (HAART). This reservoir must be eliminated for the clearance of infection. Using a cDNA library screen, we have identified methyl-CpG binding domain protein 2 (MBD2) as a regulator of HIV-1 latency. Two CpG islands flank the HIV-1 transcription start site and are methylated in latently infected Jurkat cells and primary CD4+ T cells. MBD2 and histone deacetylase 2 (HDAC2) are found at one of these CpG islands during latency. Inhibition of cytosine methylation with 5-aza-2′deoxycytidine (aza-CdR) abrogates recruitment of MBD2 and HDAC2. Furthermore, aza-CdR potently synergizes with the NF-κB activators prostratin or TNF-α to reactivate latent HIV-1. These observations confirm that cytosine methylation and MBD2 are epigenetic regulators of HIV-1 latency. Clearance of HIV-1 from infected persons may be enhanced by inclusion of DNA methylation inhibitors, such as aza-CdR, and NF-κB activators into current antiviral therapies.