Dementia due to human immunodeficiency virus (HIV) infection is the commonest cause of dementia in children, young adults and middle-aged people. Its incidence continues to rise despite the use of newer antiretroviral agents. The study of the pathogenesis of HIV dementia has lead to the discovery of novel mechanisms of neural dysfunction and toxicity, and holds promise for further discovery of new molecules and pathways involved in maintaining cerebral function and enabling dysfunction. New to the field of neurovirology is the emerging concept that proteins that are part of the virus may themselves be neurotoxic by virtue of their abilities to be either directly toxic to brain cells or may, through their actions on glial cells or macrophages, release neurotoxic products coded by the host genome. These mechanisms have been demonstrated for HIV-1 and accordingly we propose a new term, virotoxins, to describe such actions. This review provides an in-depth analysis of the pathophysiological mechanisms by which these vital and cellular products affected by HIV virotoxins cause neural dysfunction.
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