Frontal lobe neuronal injury correlates to altered function in FIV-infected cats

Citation
M. Podell et al., Frontal lobe neuronal injury correlates to altered function in FIV-infected cats, J ACQ IMM D, 22(1), 1999, pp. 10-18
Citations number
56
Categorie Soggetti
Clinical Immunolgy & Infectious Disease",Immunology
Journal title
JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY
ISSN journal
15254135 → ACNP
Volume
22
Issue
1
Year of publication
1999
Pages
10 - 18
Database
ISI
SICI code
1525-4135(19990901)22:1<10:FLNICT>2.0.ZU;2-D
Abstract
Six cats infected intravenously at 8 weeks of age with feline immunodeficie ncy virus Maryland isolate (FIV-MD), were evaluated at 8 and 14 months of a ge (6 months and 12 months postinfection, respectively) with high spatial r esolution proton magnetic resonance spectroscopy (MRS) of the frontal corte x. Two separate control cat groups were evaluated at 8 months and 16 months of age. Single voxel two-dimensional high-resolution proton magnetic reson ance imaging was performed using the PRESS sequence by selecting a 0.125 mi volume of interest in the medial frontal cortex. A significant reduction i n both N-acetylaspartate (NAA) and NAA: choline ratio was found in the FIV 14-month-old group compared with FIV 8-month-old cats, and to the respectiv e age-matched control 16-month-old cats. A negative correlation between NAA and CD4 lymphocyte count was seen in the FIV-14 group only. This group of FIV cats also exhibited a higher proportion of quantitative electroencephal ographic relative slow wave activity (RSWA) that correlated to lower NAA co ntent in the frontal cortical voxel. Although peripheral blood proviral loa d increased over time of infection, no correlation was found between provir al blood or lymph node load and NAA values. CD4 lymphocyte counts, or front al cortical RSWA. Thus, this study demonstrated that neurologic functional disruption of the frontal cortex correlated strongly with neuronal injury a nd/or loss in RV-MD-infected cats independent of peripheral proviral load. The ability to define in vivo neurodegeneration further in this animal mode l helps in understanding the neuropathogenesis of lentivirus infection, and possibly, a means to follow progression and reversibility during the initi al stages of brain infection as therapeutic agents are identified.