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Journal of Virology, May 2006, p. 4326-4335, Vol. 80, No. 9
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.9.4326-4335.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Enhanced Replication of Simian Immunodeficiency Virus Adjacent to Catecholaminergic Varicosities in Primate Lymph Nodes

Erica K. Sloan,1 Ross P. Tarara,2 John P. Capitanio,2,3 and Steve W. Cole1,4*

Department of Medicine, Division of Hematology-Oncology, UCLA School of Medicine, UCLA AIDS Institute, and Cousins Center for Psychoneuroimmunology at the UCLA Semel Institute for Neuroscience and Human Behavior, Los Angeles, California,1 California National Primate Research Center,2 Department of Psychology, University of California—Davis, Davis, California,3 Jonsson Comprehensive Cancer Center and the UCLA Molecular Biology Institute, Los Angeles, California4

Received 24 August 2005/ Accepted 25 January 2006

Clinical and in vitro studies have shown that activity of the autonomic nervous system (ANS) can stimulate lentivirus replication. To define the potential anatomical basis for this effect, we analyzed the spatial relationship between catecholaminergic neural fibers and sites of simian immunodeficiency virus (SIV) replication in lymph nodes from rhesus macaques experimentally infected with SIVmac251. Viral replication was mapped by in situ hybridization for SIV env, gag, and nef RNA, and catecholaminergic varicosities from the ANS were mapped by sucrose phosphate glyoxylic acid chemofluorescence. Spatial statistical analyses showed that the likelihood of active SIV replication increased by 3.9-fold in the vicinity of catecholaminergic varicosities (P < 0.0001). The densities of both ANS innervation and SIV replication differed across cortical, paracortical, and medullary regions of the lymph node, but analyses of each region separately continued to show increased replication of SIV adjacent to catecholaminergic varicosities. Ancillary analyses ruled out the possibility that SIV-induced alterations in lymph node architecture might create a spurious spatial association. These data support human clinical studies and in vitro molecular analyses showing that catecholamine neurotransmitters from the ANS can increase lentiviral replication by identifying a specific anatomic context for interactions between ANS neural fibers and replication of SIV in lymphoid tissue.

* Corresponding author. Mailing address: Department of Medicine, Division of Hematology-Oncology, 11-934 Factor Building, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1678. Phone: (310) 267-4243. Fax: (310) 794-9247. E-mail: coles{at}ucla.edu.

Journal of Virology, May 2006, p. 4326-4335, Vol. 80, No. 9
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.9.4326-4335.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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