Neuronal injury in simian immunodeficiency virus and other animal models of neuroAIDS

The success of antiretroviral therapy has reduced the incidence of severe neurological complication resulting from human immunodeficiency virus (HIV) infection. However, increased patient survival has been associated with an increased prevalence of protracted forms of HIV encephalitis leading to moderate cognitive impairment. NeuroAIDS remains a great challenge to patients, their families, and our society. Thus development of preclinical models that will be suitable for testing promising new compounds with neurotrophic and neuroprotective capabilities is of critical importance. The simian immunodeficiency virus (SIV)-infected macaque is the premiere model to study HIV neuropathogenesis. This model was central to the seminal work of Dr. Opendra “Bill” Narayan. Similar to patients with HIV encephalitis, in the SIV model there is injury to the synaptodendritic structure of excitatory pyramidal neurons and inhibitory calbindin-immunoreactive interneurons. This article, which is part of a special issue of the Journal of NeuroVirology in honor of Dr. Bill Narayan, discusses the most important neurodegenerative features in preclinical models of neuroAIDS and their potential for treatment development.