Impaired response to HAART in HIV-infected individuals with high autonomic nervous system activity.
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.
Cole
S W
SW
Department of Medicine, University of California, Los Angeles, CA 90095, USA. coles@nicco.sscnet.ucla.edu
Naliboff
B D
BD
Kemeny
M E
ME
Griswold
M P
MP
Fahey
J L
JL
Zack
J A
JA
D000328:Adult; D023241:Antiretroviral Therapy, Highly Active; D001341:Autonomic Nervous System / Q000503:physiopathology*; D018791:CD4 Lymphocyte Count; D015658:HIV Infections / Q000188:drug therapy* / Q000276:immunology / Q000503:physiopathology; D015497:HIV-1 / Q000187:drug effects / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000494:pharmacology; D019562:Viral Load; D014779:Virus Replication / Q000187:drug effects
D009638:Norepinephrine