This Article Full Text Full Text (PDF) Other Versions of this Article: JVI.02671-06v1 81/12/6265    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Orandle, M. S. Articles by Lackner, A. A. Search for Related Content PubMed PubMed Citation Articles by Orandle, M. S. Articles by Lackner, A. A.

Enteric Ganglionitis in Rhesus Macaques Infected with Simian Immunodeficiency Virus

Department of Pathobiological Sciences, Louisiana State University, School of Veterinary Medicine, Baton Rouge, Louisiana 70803,¹ Tulane National Primate Research Center, Tulane University Health Sciences Center, 18703 Three Rivers Road, Covington, Louisiana 70433²

Received 4 December 2006/ Accepted 21 March 2007

Gastrointestinal (GI) disease is a debilitating feature of human immunodeficiency virus (HIV) infection that can occur in the absence of histopathological abnormalities or identifiable enteropathogens. However, the mechanisms of GI dysfunction are poorly understood. The present study was undertaken to characterize changes in resident and inflammatory cells in the enteric nervous system (ENS) of macaques during the acute stage of simian immunodeficiency virus (SIV) infection to gain insight into potential pathogenic mechanisms of GI disease. Ganglia from duodenum, ileum, and colon were examined in healthy and acutely infected macaques by using a combination of routine histology, double-label immunofluorescence and in situ hybridization. Evaluation of tissues from infected macaques showed progressive infiltration of myenteric ganglia by CD3⁺ T cells and IBA1⁺ macrophages beginning as early as 8 days postinfection. Quantitative image analysis revealed that the severity of myenteric ganglionitis increased with time after SIV infection and, in general, was more severe in ganglia from the small intestine than in ganglia from the colon. Despite an abundance of inflammatory cells in myenteric ganglia during acute infection, the ENS was not a target for virus infection. This study provides evidence that the ENS may be playing a role in the pathogenesis of GI disease and enteropathy in HIV-infected people.

Published ahead of print on 28 March 2007.