Like HIV, FIV causes a chronic progressive immunodeficiency that ultimately results in the development of opportunistic infections and the death of the host.
Neurologic abnormalities are a frequent complication of both viral infections.
Our objectives are to gain a better understanding of the neuropathogenesis associated with FIV infections and to investigate various therapeutic interventions. Using cultures of feline neurons, we investigated the potential of both FIV and its envelope protein to cause neuronal damage through the excitotoxicity mechanism. Neuronal swelling and release of lactate dehydrogenase were used to measure cellular damage. We also examined the effects of FIV envelope protein on increases in intracellular concentrations of calcium mediated by glutamate receptors. Both FIV and its envelope protein significantly increased release of lactate dehydrogenase from cultured neurons.