Neurological disease is recognized prior to overt acquired immunodeficiency syndrome in HIV infection. The mechanism of early neurologic injury needs study to address basic questions of neuro-AIDS pathogenesis. Whether the neurological deficits seen in AIDS is due to cumulative injury beginning in the asymptomatic phase, or whether separate mechanisms are activated at later infection stages can be determined only when early mechanisms are known. Clinical development of FIV infection closely models HIV disease. The project hypothesis is that persistent alterations in glutamate metabolism in the brain cause progressive neuronal injury during the asymptomatic phase of FIV infection of the cat.
Four specific aims will 1) study the kinetics of neuronal loss in asymptomatic phase FIV infection with unbiased methods, 2) use quantitative polymerase chain reaction (PCR) to show brain viral load is constantly low in this phase, 3) analyze RNA and protein expression of astrocytic glutamate transporter GLT-1, and 4) examine a neural culture model for energy deficit.

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
Research Scientist Development Award - Research & Training (K01)
Project #
5K01RR000154-03
Application #
6639829
Study Section
National Center for Research Resources Initial Review Group (RIRG)
Program Officer
Harding, John D
Project Start
2001-04-01
Project End
2004-03-31
Budget Start
2003-04-01
Budget End
2004-03-31
Support Year
3
Fiscal Year
2003
Total Cost
$101,909
Indirect Cost
Name
Ohio State University
Department
Veterinary Sciences
Type
Schools of Veterinary Medicine
DUNS #
071650709
City
Columbus
State
OH
Country
United States
Zip Code
43210
Terrell, Kimberly A; Rasmussen, Terri A; Trygg, Cyndi et al. (2007) Molecular beacon genotyping for globoid cell leukodystrophy from hair roots in the twitcher mouse and rhesus macaque. J Neurosci Methods 163:60-6