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Mitochondrial dysfunction in HIV-induced peripheral neuropathy.

Ricardo H Roda1, Ahmet Hoke2

  • 1Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, United States.

International Review of Neurobiology
|June 19, 2019
PubMed
Summary
This summary is machine-generated.

Human Immunodeficiency Virus (HIV) infection can cause peripheral neuropathy by disrupting mitochondrial function. This dysfunction affects energy production and involves toxic viral proteins and treatments, impacting neuronal health.

Keywords:
HIV neuropathyMitochondrial neuropathygp120

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Virology

Background:

  • Mitochondria are crucial for neuronal energy production and calcium balance.
  • Mitochondrial dysfunction is implicated in various neuropathies.
  • HIV infection is a known risk factor for peripheral neuropathy, even with treatment.

Purpose of the Study:

  • To explore how HIV infection, its products, and treatments affect mitochondrial function in neurons.
  • To investigate the neurotoxic effects of HIV's gp120 protein on mitochondria.
  • To examine the unexplored role of mitochondria-endoplasmic reticulum interactions in HIV neuropathy.

Main Methods:

  • Review of existing literature on HIV, mitochondrial function, and neuropathy.
  • Analysis of the impact of viral proteins (gp120) on mitochondrial DNA replication.
  • Discussion of potential disruption in mitochondria-endoplasmic reticulum communication.

Main Results:

  • HIV infection and associated factors can lead to abnormal mitochondrial function.
  • Viral gp120 protein exhibits neurotoxic effects impacting mitochondria.
  • Mitochondrial DNA replication may be impaired.

Conclusions:

  • HIV-related neuropathy involves complex mitochondrial dysfunction.
  • Further research into mitochondria-endoplasmic reticulum interactions is warranted for understanding and treating HIV neuropathy.