Infection with human immunodeficiency virus (HIV) commonly results in neurologic disease termed the AIDS dementia complex (ADC) Neuronal loss and injury have been found in the HIV-infected brain, but the underlying mechanisms are poorly understood The simian immunodeficiency virus (SIV) infected macaque is an excellent model for HIV infection, but neuronal loss has not been demonstrated To determine whether neuronal damage occurs in the SIV-infected macaque we quantified the neuronal marker n-acetylaspartate (NAA) using proton magnetic resonance spectroscopy in brain extracts of control and SIV infected macaques and correlated these findings with histologic analyses We found reduced NAA in the SIV-infected animals compared to controls (2 94+1 37 versus 6 21+1 73 mols/g wet weight; p=0 004) A significant decrease in NAA was also found in SIV-infected animals sacrificed in the acute stages of infection We conclude that SIV infection of rhesus macaques re sults in neuronal damage that is demonstrable soon after infection Publications Tracey I, Lane J, Chang I, Navia B, Lackner A, Gonzalez RG 1H-MRS reveals neuronal injury in simian immunodeficiency virus macaque model Journal of Acquired Immune Deficiency Syndrome Human Retroviruses 15:21-27, 1997 Cheng LL, Ma MJ, Becerra L, Ptak T, Tracey I, Lackner A, Gonzalez RG Quantitative neuropathology by high resolution magic angle spinning proton magnetic resonance spectroscopy PNAS, 94:6408-6413, 1997

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
Primate Research Center Grants (P51)
Project #
5P51RR000168-41
Application #
6591327
Study Section
Project Start
2002-05-01
Project End
2003-04-30
Budget Start
1997-10-01
Budget End
1998-09-30
Support Year
41
Fiscal Year
2002
Total Cost
$111,112
Indirect Cost
Name
Harvard University
Department
Type
DUNS #
082359691
City
Boston
State
MA
Country
United States
Zip Code
02115
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Ma, Qi; Ruan, Hongyu; Peng, Lisheng et al. (2017) Proteasome-independent polyubiquitin linkage regulates synapse scaffolding, efficacy, and plasticity. Proc Natl Acad Sci U S A 114:E8760-E8769
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