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
Categorie Soggetti
Clinical Immunolgy & Infectious Disease",Immunology
Journal title
JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY
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.