NYMC Faculty Publications
Human Immunodeficiency Virus-1/Simian Immunodeficiency Virus Infection Induces Opening of Pannexin-1 Channels Resulting in Neuronal Synaptic Compromise: A Novel Therapeutic Opportunity to Prevent NeuroHIV
Author Type(s)
Faculty
Journal Title
Journal of Neurochemistry
First Page
500
Last Page
521
Document Type
Article
Publication Date
7-2021
Department
Cell Biology and Anatomy
Abstract
In healthy conditions, pannexin-1 (Panx-1) channels are in a close state, but in several pathological conditions, including human immunodeficiency virus-1 (HIV) and NeuroHIV, the channel becomes open. However, the mechanism or contribution of Panx-1 channels to the HIV pathogenesis and NeuroHIV is unknown. To determine the contribution of Panx-1 channels to the pathogenesis of NeuroHIV, we used a well-established model of simian immunodeficiency virus (SIV) infection in macaques (Macaca mulatta) in the presence of and absence of a Panx-1 blocker to later examine the synaptic/axonal compromise induced for the virus. Using Golgi's staining, we demonstrated that SIV infection compromised synaptic and axonal structures, especially in the white matter. Blocking Panx-1 channels after SIV infection prevented the synaptic and axonal compromise induced by the virus, especially by maintaining the more complex synapses. Our data demonstrated that targeting Panx-1 channels can prevent and maybe revert brain synaptic compromise induced by SIV infection.
Recommended Citation
Gorska, A., Donoso, M., Valdebenito, S., Prideaux, B., Queen, S., Scemes, E., Clements, J., & Eugenin, E. (2021). Human Immunodeficiency Virus-1/Simian Immunodeficiency Virus Infection Induces Opening of Pannexin-1 Channels Resulting in Neuronal Synaptic Compromise: A Novel Therapeutic Opportunity to Prevent NeuroHIV. Journal of Neurochemistry, 158 (2), 500-521. https://doi.org/10.1111/jnc.15374
