The Unresolved Biology of ME/CFS: Viruses, Bacteria, and Mitochondrial Damage

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In my previouspost, I examined two unresolved historical questions: first, how long it took the scientific community to confirm Dr. Carleton Gajdusek’s discovery of Kuru; and second, whether Gajdusek’s work would ever have been validated had Stanley Prusiner’s scrapie research not led to the development of the “protein-only” prion hypothesis. This raises an important parallel question: are we now facing a similar situation with ME/CFS?

My central concern is whether ME/CFS is primarily associated with a viral or bacterial origin. To date, scientific research has focused predominantly on viral explanations, while bacterial mechanisms have received comparatively limited attention as potential contributors or vectors.

Another important issue is whether bacteria can reside within mitochondria, leading to mitochondrial rupture and eventual cell death. Current evidence suggests that this is indeed possible. Many pathogenic bacteria are known to exploit mitochondrial functions in ways that enhance their survival and dissemination, and such interactions are increasingly recognized as significant mechanisms of pathogenicity.

Tuberculosis provides a useful example. In latent TB, the immune system walls off the bacteria, allowing them to persist in a dormant state for years. Viral infections may later contribute to reactivation by weakening immune defenses. Likewise, influenza infections can predispose individuals to secondary bacterial pneumonia, illustrating the complex interplay between viral and bacterial pathogens.

This also recalls the repeated waves of deadly epidemics that swept across Europe between 1837 and 1901. Among the most feared were cholera, tuberculosis—the leading cause of death at the time—smallpox, typhoid fever, and scarlet fever. These historical outbreaks demonstrate the profound and long-term biological consequences infectious diseases can have on populations.

Bacterial infections are capable of inducing genetic mutations in infected cells, and if such mutations are passed to subsequent generations of cells, long-term pathological consequences may result. Viral infections may also contribute by triggering prolonged inflammatory responses and releasing toxic byproducts that damage DNA and interfere with normal cellular repair mechanisms.

For this reason, the exploration of genetic markers may be important in linking past and present disease mechanisms, potentially leading to a more precise understanding of ME/CFS and its underlying biological pathways.

Since subsequent studies failed to replicate Dr. Elaine DeFreitas’s findings—largely because the same experimental procedures were not followed—the question remains unresolved as to what precisely she identified. It is therefore worth considering whether her observations could now be re-examined and potentially verified using today’s far more advanced microscopy and molecular analytical technologies.

References:
Control of host mitochondria by bacterial pathogens  https://www.sciencedirect.com/science/article/abs/pii/S0966842X21002377?utm_source=chatgpt.com

Interactions between bacterial pathogens and mitochondrial cell death pathways https://www.nature.com/articles/nrmicro2421?utm_source=chatgpt.com

The effect of oral bacterial infection on DNA damage response in host cells: https://pmc.ncbi.nlm.nih.gov/articles/PMC10408462/

Tampering of Viruses and Bacteria with Host DNA Repair: Implications for Cellular Transformation https://pmc.ncbi.nlm.nih.gov/articles/PMC7826954/

A very interesting read: “Are Victorian diseases making a comeback?”
https://ukhsa.blog.gov.uk/2019/03/28/are-victorian-diseases-making-a-comeback/


© 2000-2030 Sieglinde W. Alexander. All writings by Sieglinde W. Alexander have a five-year copyright. Library of Congress Card Number: LCN 00-192742 ISBN: 0-9703195-0-9 

 

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