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Deregulation of microRNAs by HIV-1 Vpr protein leads to the development of neurocognitive disorders

Ruma Mukerjee1, J Robert Chang, Luis Del Valle

  • 1Department of Neurology, Molecular Studies of Neurodegenerative Diseases Laboratory, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA.

The Journal of Biological Chemistry
|August 6, 2011
PubMed

Insights

The HIV-1 viral protein R (Vpr) disrupts neuron function by altering microRNA and gene expression, leading to neurocognitive disorders. This protein causes calcium imbalance, oxidative stress, and synaptic damage in neurons.

Area of Science:

  • Neuroscience
  • Virology
  • Molecular Biology

Background:

  • HIV-1 infection is linked to neurocognitive disorders and neuronal dysfunction.
  • Viral proteins released from infected cells, not direct infection, are implicated in neuronal damage.
  • The precise mechanisms by which HIV-1 proteins cause neurotoxicity are not fully understood.

Purpose of the Study:

  • To investigate the role of HIV-1 viral protein R (Vpr) in neuronal dysfunction.
  • To elucidate the cellular mechanisms underlying Vpr-induced neurotoxicity.
  • To identify specific molecular pathways, including microRNAs, affected by Vpr.

Main Methods:

  • Utilized a human neuronal cell line (SH-SY5Y) and primary neuronal cultures.
  • Treated neurons with recombinant Vpr proteins.
  • Performed microRNA and gene array assays to analyze molecular changes.
  • Assessed cellular functions including calcium homeostasis, oxidative stress, mitochondrial function, and synaptic integrity.

Main Results:

  • Vpr uptake by neurons led to calcium homeostasis deregulation and endoplasmic reticulum-calcium release.
  • Vpr activated the oxidative stress pathway and caused mitochondrial dysfunction.
  • Synaptic retraction was observed in Vpr-treated neurons.
  • Vpr significantly altered microRNA levels (e.g., miR-34a) and their target genes (e.g., CREB) in neurons.

Conclusions:

  • HIV-1 Vpr plays a critical role in neuronal dysfunction and neurocognitive disorders.
  • Vpr induces neurotoxicity by deregulating microRNA and target gene expression in neurons.
  • Understanding Vpr's molecular targets provides insight into HIV-associated neurological complications.

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