This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Bissel, S. J. Articles by Wiley, C. A. Search for Related Content PubMed PubMed Citation Articles by Bissel, S. J. Articles by Wiley, C. A.

(American Journal of Pathology. 2006;168:1553-1569.)
© 2006 American Society for Investigative Pathology

Longitudinal Analysis of Monocyte/Macrophage Infection in Simian Immunodeficiency Virus-Infected, CD8⁺ T-Cell-Depleted Macaques that Develop Lentiviral Encephalitis

Stephanie J. Bissel^*, Guoji Wang, Anita M. Trichel, Michael Murphey-Corb and Clayton A. Wiley

From the Department of Infectious Diseases and Microbiology,^* Graduate School of Public Health, and the Departments of Pathology and Molecular Genetics and Biochemistry, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania

The histopathological hallmark of lentiviral-associated encephalitis is an abundance of infected and activated macrophages. Why a subset of infected hosts develops lentiviral encephalitis and others do not is unknown. Using a CD8⁺ T-cell depletion model of simian immunodeficiency virus (SIV)-infected rhesus macaques, we examined the relationship between peripheral SIV infection of monocytes/macrophages and the development of encephalitis. At the same time that cerebral spinal fluid viral load increased in macaques that developed encephalitis, we observed that monocyte-derived macrophages from these macaques produced more virus than those from macaques that did not develop encephalitis. However, during the course of infection, the number of blood monocyte-associated SIV DNA copies did not distinguish macaques that developed simian immunodeficiency virus encephalitis from macaques that did not develop encephalitis. Paradoxically, in this model, macaques that developed encephalitis had fewer SIV-infected macrophages in lungs and thymus at postmortem than macaques that did not develop encephalitis. These findings suggest that inherent differences in host monocyte viral production are related to development of encephalitis.

This article has been cited by other articles:

				D. L. Kolson YKL-40: A Candidate Biomarker for Simian Immunodeficiency Virus and Human Immunodeficiency Virus Encephalitis? Am. J. Pathol., July 1, 2008; 173(1): 25 - 29. [Abstract] [Full Text] [PDF]

				D. Bonneh-Barkay, S. J. Bissel, G. Wang, K. N. Fish, G. C.B. Nicholl, S. W. Darko, R. Medina-Flores, M. Murphey-Corb, P. A. Rajakumar, J. Nyaundi, et al. YKL-40, a Marker of Simian Immunodeficiency Virus Encephalitis, Modulates the Biological Activity of Basic Fibroblast Growth Factor Am. J. Pathol., July 1, 2008; 173(1): 130 - 143. [Abstract] [Full Text] [PDF]

				S. Venneti, D. Bonneh-Barkay, B. J. Lopresti, S. J. Bissel, G. Wang, C. A. Mathis, M. Piatak Jr., J. D. Lifson, J. O. Nyaundi, M. Murphey-Corb, et al. Longitudinal in Vivo Positron Emission Tomography Imaging of Infected and Activated Brain Macrophages in a Macaque Model of Human Immunodeficiency Virus Encephalitis Correlates with Central and Peripheral Markers of Encephalitis and Areas of Synaptic Degeneration Am. J. Pathol., June 1, 2008; 172(6): 1603 - 1616. [Abstract] [Full Text] [PDF]

				S. J. Bissel, G. Wang, D. Bonneh-Barkay, A. Starkey, A. M. Trichel, M. Murphey-Corb, and C. A. Wiley Systemic and Brain Macrophage Infections in Relation to the Development of Simian Immunodeficiency Virus Encephalitis J. Virol., May 15, 2008; 82(10): 5031 - 5042. [Abstract] [Full Text] [PDF]

				C. C. Clay, D. S. Rodrigues, Y. S. Ho, B. A. Fallert, K. Janatpour, T. A. Reinhart, and U. Esser Neuroinvasion of Fluorescein-Positive Monocytes in Acute Simian Immunodeficiency Virus Infection J. Virol., November 1, 2007; 81(21): 12040 - 12048. [Abstract] [Full Text] [PDF]