CORTICAL CELL LOSS IN ASYMPTOMATIC CATS EXPERIMENTALLY INFECTED WITH FELINE IMMUNODEFICIENCY VIRUS

Specific pathogen-free cats experimentally infected with feline immuno deficiency virus (FIV) were used to evaluate the development of centra l nervous system changes during the asymptomatic stages of viral infec tion, The brains of asyptomatic cats were examined at postinoculation times ranging from 8 weeks to 3 years for changes in neuron density, g lutamate receptor density, and synaptophysin immunoreactivity. At 2-3 years postinoculation a small decrease in neuronal density was found i n layers 2-3 and layer 5 of the frontal cortex (-14.4%), parietal cort ex (-18.1%), and striatum (-29.5%), The only other indications of path ology within these regions were a mild diffuse astrogliosis, occasiona l microglial nodules, and the accumulation of satellite cells around s elected neurons, An average loss of large neurons of 56-68% was seen i n the cortex of four random source cats euthanized with AIDS, These va lues conrasted with the absence of any significant cell loss in FIV-in fected cats 18 weeks after inoculation or FIV-negative controls, The l oss of neurons in the asymptomatic cats showed a significant positive correlation with a decrease in the blood CD4:CD8 ratios. Morphometric evaluation of synaptic terminal densities immunocytochemically stained with synaptophysin revealed a significant increase in the asymptomati c cats at 2-3 years postinoculation that correlated negatively with th e CD4:CD8 ratios, Random source AIDS cats showed a 34% decrease in syn aptophysin-immunoreactive profiles, Glutamate binding in the cortex di d not change significantly in the asymptomatic cats (4-7% decline), Th us, experimentally infected specific pathogen-free cats show a loss of cortical neurons similar to what has been observed in postmortem stud ies of humans infected with HIV. The detection of neuronal loss during the asymptomatic stage of disease and the correlation with the periph eral CD4:CD8 cell ratios indicate that neurodegeneration may progress in parallel with peripheral disease.