HIV immune complexes prevent excitotoxicity by interaction with NMDA receptors.

ABSTRACT:

Purpose

Human immunodeficiency virus-1 (HIV)-associated neurocognitive disorder (HAND) is a neurodegenerative disease for which there is no available neuroprotective therapy. Viral proteins, such as Tat, have been implicated as agents of neurotoxicity via multiple mechanisms, including effects by directly binding to the NMDA receptor. We evaluated the ability of the immune response against Tat to modulate neurotoxicity at glutamate receptors.

Methods

Neurotoxicity was measured in primary neuronal-glial cultures and in hippocampal slice cultures. We used immunoprecipitation experiments to demonstrate interaction between Tat, NMDA receptor, and anti-Tat antibody. Using known structures of Tat and NMDA receptors, we developed a model of their interactions.

Results

Antibo

SUBMITTER: Rumbaugh JA 

PROVIDER: S-EPMC3556339 | biostudies-literature | 2013 Jan

REPOSITORIES: biostudies-literature