Herpesvirus Infection as a Systemic Pathological Axis in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (Nunes, Kell & Pretorius, preprint)

[Murph]

Posted Date: 19 January 2024

Herpesvirus Infection as a Systemic Pathological Axis in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
Jean M Nunes 1 and Douglas B. Kell 1,2,3,* and Etheresia Pretorius 1,2,*

1 Department of Physiological Sciences, Faculty of Science, Stellenbosch University, Stellenbosch, Private
Bag X1 Matieland, 7602, South Africa
2 Department of Biochemistry, Cell and Systems Biology, Institute of Systems, Molecular and Integrative
Biology, Faculty of Health and Life Sciences, University of Liverpool, Crown St, Liverpool L69 7ZB, UK
3 The Novo Nordisk Foundation Center for Biosustainability, Building 220, Chemitorvet 200, Technical
University of Denmark, 2800 Kongens Lyngby, Denmark

Abstract: Understanding the pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue
Syndrome (ME/CFS) is critical for advancing treatment options. This review explores the novel
hypothesis that herpesviruses' infection of endothelial cells (ECs) may underlie ME/CFS
symptomatology. We review evidence linking herpesviruses to persistent EC infection and the
implications for endothelial dysfunction, encompassing blood flow regulation, coagulation, and
cognitive impairment – symptoms consistent with ME/CFS and Long COVID. The paper provides
a synthesis of current research on herpesvirus latency and reactivation, detailing the impact on ECs
and subsequent systemic complications, including latent modulation and long-term maladaptation.

We suggest that the chronicity of ME/CFS symptoms and the multisystemic nature of the disease
may be partly attributable to herpesvirus-induced endothelial maladaptation. Our conclusions
underscore the necessity for further investigation into the prevalence and load of herpesvirus
infection within ECs of ME/CFS patients. This review offers a conceptual advance by proposing an
endothelial infection model as a systemic mechanism contributing to ME/CFS, steering future
research towards potentially unexplored avenues in understanding and treating this complex
syndrome.

doi: 10.20944/preprints202401.1486.v1

 

[Murph]

This is a pure hypothesis paper. It makes the very reasonable argument that if we've got endothelial dysfunction and herpesvirus infection maybe the problem is ebv infection of endothelial cells.

It's a nice tight idea but ideas are cheap. Let's hope some resources are forthcoming for them to get what really matters, which is evidence.

 

[Vladimir]

From my personal experience, herpes is merely a consequence of the immune disfunction caused by ME. And nothing suggests the opposite.

 

[Forummember9922]

I think people should be keeping an eye on upcoming therapeutic vaccines for HSV and EBV. There is a big money driven race by big pharma.

If these come out, are effective at treating their targets, and do nothing for CFS, that is still valuable data.

 

[Wishful]

It probably fails my "can switch state over the space of minutes" test for hypotheses. I haven't noticed any effects I consider due to blood flow problems. If ME symptoms were due to blood flow problems, wouldn't symptom severity change between resting states and highly active states, or due to any other factors that affect blood pressure and flow?

I haven't noticed any changes in my ME severity when I have an active cold sore, for whatever that's worth in regards to the hypothesis.

 

[heapsreal]

From my personal experience, herpes is merely a consequence of the immune disfunction caused by ME. And nothing suggests the opposite.

I think so too. These infections are well controlled by normal non cfs people but in cfs people with low nk function etc, they can more easily reactivate.

I think the initial triggering infection that many get, some how breaks or disrupts the immune system. The triggering infection could be anything but it's also possible if one of the herpes viruses was the trigger, it could still be active??? And other dormant infections could also reactivate, bacterial or viral, as well as easier to pick up new infections. And or the triggering infection could have caused an autoimmune response.