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目的探讨高效抗逆转录病毒治疗(HAART)病毒学抑制后HIV-1嗜性的转换。方法提取治疗前和治疗48周患者的外周血单个核细胞中基因组DNA,对HIV-1 env基因的C2-V5区进行(nested-PCR)扩增和测序。基于V3区碱基序列,通过Geno2pheno软件预测HIV-1的嗜性。结果经HAART 48周后,其中11例患者病毒得到完全抑制,血浆病毒载量低于检测下限(20拷贝/ml),CD4+T淋巴细胞计数显著增加(均值自208 cells/ml上升至48周的418 cells/ml,Z=-2.934,P=0.001)。其中1例患者出现病毒嗜性由CCR5向CXCR4的转换,另外10例患者保持CCR5嗜性,V3环所带正电荷(Z=-1.000,P=0.317)和净电荷(Z=-1.000,P=0.317)均未发生显著性改变。结论 HAART后病毒获得抑制,可能延缓CXCR4嗜性病毒株的出现,这些患者可考虑使用CCR5拮抗剂作为优化方案的选择。
Objective To investigate the change of HIV-1 tropism after virological suppression of highly active antiretroviral therapy (HAART). Methods Genomic DNA was extracted from peripheral blood mononuclear cells of patients before and 48 weeks after treatment. The C2-V5 region of HIV-1 env gene was amplified by nested-PCR and sequenced. Based on the V3 region base sequence, the tropism of HIV-1 was predicted by Geno2 pheno software. Results After HAART for 48 weeks, the virus was completely inhibited in 11 of them and the plasma viral load was lower than the lower limit of detection (20 copies / ml). CD4 + T lymphocyte count increased significantly (mean value increased from 208 cells / ml to 48 weeks Of 418 cells / ml, Z = -2.934, P = 0.001). One patient developed CCR5 to CXCR4 conversion, and the other 10 patients maintained CCR5 tropism with V3 (positive) (Z = -1.000, P = 0.317) and net charge (Z = -1.000, P = 0.317) did not change significantly. Conclusions Inhibition of HAART after infection may delay the emergence of CXCR4 tropic virus strains. These patients may consider the use of CCR5 antagonists as an option for optimization.