A central role for glial CCR5 in directing the neuropathological interactions of HIV-1 Tat and opiates

201848 citationsJournal Articlegold Open Access

Authors

Sarah Kim-Hellmuth · Virginia Commonwealth University

Yun K. Hahn · Virginia Commonwealth University

Elizabeth M. Podhaizer · Virginia Commonwealth University

Virginia D. McLane · Virginia Commonwealth University

Shiping Zou · Computercraft (United States)

Kurt F. Hauser · Virginia Commonwealth University

Pamela E. Knapp

Abstract

Our results suggest a critical role for glial CCR5 in mediating neurotoxic effects of HIV-1 Tat and morphine interactions on neurons. A shift in the proBDNF/BDNF ratio that favors neurotrophic support may occur when glial CCR5 signaling is blocked. Some neuroprotection occurred only in the presence of morphine, suggesting that loss of CCR5 may fundamentally change signaling through the MOR in glia.

Topics & Keywords

HIV Research and Treatment Neuroinflammation and Neurodegeneration Mechanisms RNA Interference and Gene Delivery

UN Sustainable Development Goals

Good health and well-being

Publication Details

Published in: Journal of Neuroinflammation

Volume 15, Issue 1, pp. 285-285

DOI: 10.1186/s12974-018-1320-4

Field-Weighted Citation Impact: 3.35