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J. Virol. doi:10.1128/JVI.02671-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

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; Tulane National Primate Research Center, Tulane University Health Science Center, 18703 Three Rivers Road, Covington, LA 70433

^* To whom correspondence should be addressed. Email: morandle{at}vetmed.lsu.edu.

	Abstract

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 current 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 infection (SIV) to gain insight into potential pathogenic mechanisms of GI disease. Ganglia from duodenum, ileum and colon were examined in healthy and acutely infected macaques 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 early as 8 days post infection. Quantitative image analysis revealed that the severity of myenteric ganglionitis increased with time following SIV infection and, in general, was more severe in ganglia from the small intestine when compared with 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.