Signaling pathways to neuronal damage and apoptosis in human immunodeficiency virus type 1–associated dementia: Chemokine receptors, excitotoxicity, and beyond

Abstract

Dementia can occur as a debilitating consequence of human immunodeficiency virus-1 (HIV-1) infection. The neuropathology incited by HIV infection involves activation of chemokine receptors, inflammatory factors, and N-methyl-D-aspartate (NMDA) receptor–mediated excitotoxicity, all of which can activate several downstream mechanisms. This article discusses recently identified pathways to neuronal damage triggered by HIV-1 and efforts aimed at development of applicable therapeutic intervention.