Further characterization of the spatial learning deficit in the human immunodeficiency virus-1 transgenic rat.

Human immunodeficiency virus (HIV)-associated dementia (HAD) encompasses a spectrum of cognitive and motor deficits resulting from the progression of central nervous system abnormalities caused by the HIV-1 virus. With the advent of highly active antiretroviral therapy (HAART), these deficits have become milder, but more prevalent as the population of HIV-positive individuals ages. Mild impairment in cognition has also been identified in asymptomatic HIV-1 patients. The noninfectious HIV-1 transgenic (Tg) rat recently developed to study the pathogenesis of acquired immunodeficiency syndrome (AIDS) may also be useful for the study of the early and chronic effects of HIV-1 on learning and cognition. In a previous study, we demonstrated that HIV-1Tg rats show a deficit in learning how to swim to a hidden platform in a modified water maze task compared to normal and transgenic controls. In the present study, we replicate this result and demonstrate that HIV-1Tg rats also show a significant deficit in reversal learning and new strategy learning. These results indicate that the HIV-1Tg rat is a promising model in which to study the neuropathogenic mechanisms that can cause cognitive deficits in patients with HAD as well as asymptomatic HIV-positive individuals.