Format

Send to

Choose Destination
J Neurovirol. 2019 Jun;25(3):301-312. doi: 10.1007/s13365-019-00737-y. Epub 2019 Mar 8.

HIV-associated neurodegeneration: exploitation of the neuronal cytoskeleton.

Author information

1
Department of Pharmacology & Physiology, Georgetown University Medical Center, 3970 Reservoir Rd NW, Washington, DC, 20057, USA.
2
Department of Neuroscience, Georgetown University Medical Center, 3970 Reservoir Rd NW, Washington, DC, 20057, USA.
3
Department of Pharmacology & Physiology, Georgetown University Medical Center, 3970 Reservoir Rd NW, Washington, DC, 20057, USA. moccheti@georgetown.edu.
4
Department of Neuroscience, Georgetown University Medical Center, 3970 Reservoir Rd NW, Washington, DC, 20057, USA. moccheti@georgetown.edu.

Abstract

Human immunodeficiency virus-1 (HIV) infection of the central nervous system damages synapses and promotes axonal injury, ultimately resulting in HIV-associated neurocognitive disorders (HAND). The mechanisms through which HIV causes damage to neurons are still under investigation. The cytoskeleton and associated proteins are fundamental for axonal and dendritic integrity. In this article, we review evidence that HIV proteins, such as the envelope protein gp120 and transactivator of transcription (Tat), impair the structure and function of the neuronal cytoskeleton. Investigation into the effects of viral proteins on the neuronal cytoskeleton may provide a better understanding of HIV neurotoxicity and suggest new avenues for additional therapies.

KEYWORDS:

Actin; BDNF; Microtubules; Neurodegeneration; Tat; gp120

PMID:
30850975
PMCID:
PMC6635009
[Available on 2020-06-01]
DOI:
10.1007/s13365-019-00737-y

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center