Mitochondrial Dysfunction in Aging, HIV, and Long COVID: Mechanisms and Therapeutic Opportunities

María Victoria Delpino1, Jorge Quarleri1

  • 1Laboratorio de Inmunopatología Viral, Instituto de Investigaciones Biomédicas en Retrovirus y Sida (INBIRS), Universidad de Buenos Aires, Consejo de Investigaciones Científicas y Técnicas (CONICET), Buenos Aires 1121, Argentina.

PubMed

Insights

A unified mitochondrial view reveals shared aging, HIV, and long COVID mechanisms. Emerging organelle therapies offer new treatment avenues for these interconnected conditions.

Area of Science:

  • Mitochondrial biology
  • Aging research
  • Infectious diseases
  • Post-viral syndromes

Background:

  • Mitochondrial dysfunction is a common pathway in aging, HIV, and long COVID.
  • Independent treatment approaches may overlook shared pathogenic mechanisms.

Purpose of the Study:

  • To explore a unified mitochondrial perspective on aging, HIV, and long COVID.
  • To identify shared mechanisms and therapeutic vulnerabilities.
  • To review emerging organelle-based therapies.

Main Methods:

  • Literature review of current evidence on mitochondrial changes.
  • Examination of shared mechanisms: oxidative stress, mitophagy, mtDNA damage, metabolic reprogramming.
  • Analysis of emerging therapeutic strategies: mitochondrial transfer, transplantation, mtDNA correction.

Main Results:

  • Mitochondrial dysfunction drives energy failure and chronic inflammation in aging, HIV, and long COVID.
  • Shared mechanisms include oxidative stress, impaired mitophagy, mtDNA damage, and metabolic reprogramming.
  • New therapies like mitochondrial transfer show preclinical and clinical proof-of-concept.

Conclusions:

  • A unified mitochondrial perspective highlights interconnectedness between aging, HIV, and long COVID.
  • Organelle-based therapies present promising, yet challenging, future treatment options.
  • Further research is needed on safety, durability, and translation of these novel therapies.

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