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,§
,§,§
*
University of California at Los Angeles (UCLA) AIDS Institute,
Center for Interdisciplinary Research in Immunology and Disease, and Departments of
Medicine,
§
Microbiology, Immunology, and Molecular Genetics, and
¶
Pathology and Laboratory Medicine, UCLA School of Medicine, Los Angeles, CA 90095
To explore the role of sympathetic nervous system activation in HIV
pathogenesis, we examined the effect of the neuroeffector molecule
norepinephrine (NE) on HIV-1 replication in quiescently infected PBMCs
that were subsequently activated with Abs to CD3 and CD28. NE
accelerated HIV-1 replication at concentrations ranging from
10-8 to 10-5 M. This effect could be
mimicked by protein kinase A (PKA) activators (forskolin or
dibutyryl-cAMP) and abrogated by ß-adrenoreceptor antagonists or the
PKA inhibitor rp-cAMP, indicating transduction via the adrenoreceptor
signaling pathway. NE reduced cellular activation and altered the
production of several HIV-modulating cytokines: IL-10 and IFN-
were
markedly suppressed; TNF-
, IL-1ß, IL-2, IL-4, and IL-6 were mildly
suppressed; and levels of IL-12 were not significantly altered. The
addition of either exogenous IFN- or IL-10 abrogated the effect of
NE on virus production. Thus PKA-dependent suppression of cytokine
production appears to mediate the enhancement of HIV-1 replication by
NE.
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