Impaired response to HAART in HIV-infected individuals with high autonomic nervous system activity
Impaired response to HAART in HIV-infected individuals with high autonomic nervous system activity
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DOI：
10.1073/pnas.221134198
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发表时间：
2001-10-23
影响因子：
11.1
通讯作者：
Zack, JA
中科院分区：
文献类型：
--
作者：
Cole, SW;Naliboff, BD;Zack, JA
神经递质在体外可加速HIV - 1的复制，这使我们去研究自主神经系统（ANS）活动的差异是否可能促进接受高效抗逆转录病毒疗法治疗的患者体内HIV - 1的残余复制。在高效抗逆转录病毒疗法治疗前自主神经系统活动持续处于高水平的患者，在3 - 11个月的治疗期间，血浆病毒载量的抑制效果较差，CD4(+) T细胞的恢复情况也较差。自主神经系统活动与可能影响发病机制的人口统计学或行为特征无关。然而，自主神经系统神经递质去甲肾上腺素通过趋化因子受体上调和增强病毒基因表达，在体外增强了HIV - 1的CCR5嗜性和CXCR4嗜性毒株的复制，这表明神经活动可能直接促进残余病毒的复制。
Neurotransmitters can accelerate HIV-1 replication in vitro, leading us to examine whether differences in autonomic nervous system (ANS) activity might promote residual HIV-1 replication in patients treated with highly active antiretroviral therapy. Patients who showed constitutively high levels of ANS activity before highly active antiretroviral therapy experienced poorer suppression of plasma viral load and poorer CD4(+) T cell recovery over 3-11 months of therapy. ANS activity was not related to demographic or behavioral characteristics that might influence pathogenesis. However, the ANS neurotransmitter norepinephrine enhanced replication of both CCR5- and CXCR4-tropic strains of HIV-1 in vitro via chemokine receptor up-regulation and enhanced viral gene expression, suggesting that neural activity may directly promote residual viral replication.