Impaired response to HAART in HIV-infected individuals with high autonomic nervous system activity

被引：97

作者：

Cole, SW ^{[1
]}

Naliboff, BD

Kemeny, ME

Griswold, MP

Fahey, JL

Zack, JA

机构：

[1] Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90095 USA

[2] Univ Calif Los Angeles, Dept Microbiol Mol Genet & Immunol, Los Angeles, CA 90095 USA

[3] Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA

[4] Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90095 USA

[5] Univ Calif Los Angeles, AIDS Inst, Los Angeles, CA 90095 USA

[6] Vet Adm Greater Los Angeles Area Healthcare Syst, Los Angeles, CA 90073 USA

[7] Consolidated Lab Serv, Van Nuys, CA 91406 USA

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2001年 / 98卷 / 22期

关键词：

D O I：

10.1073/pnas.221134198

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 [理学]; 0710 [生物学]; 09 [农学];

摘要：

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.

引用

页码：12695 / 12700

页数：6

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