I haven't read the study, but I note it says 'particular Herpes simplex Virus variants'. I think our understanding of the variability in bacteria, protozoa and probably viruses too is not great at present. I guess it's possible that, just like the human papilloma virus, there is a big variability in the potential of individual strains of herpes viruses to cause long term diseases. If researchers don't look at the strain level, important information might be missed.
I agree strains are important for further research, but don't kill a good idea with more detail than is needed to appreciate why the idea is good. If having HSV1 is sufficient to generate a 250% higher Alzheimer's risk, that's interesting by itself, without any discussion about strains. They tested at least four HSV1 antivirals in the Taiwan study, and they all had dramatic impacts on Alzheimer's risk.
There are at least eight types of Herpes virus, and I believe the Taiwan study was restricted to HSV1, which other studies show can reside in the cerebral cortex as a chronic infection. Other herpes variants - like EBV and CMV - reside in other parts of the CNS. CMV I have read can inhibit your neuronal stem cells from developing, so you would potentially have a double whammy with HSV1 and CMV: HSV1 might create a chronic infection that atrophies your cortex, while CMV prevents much of the repair and regeneration from working optimally.
I'm not saying we should all be taking anti-virals though. About a year into my ME/CFS, I constantly had cold sores, as in, as soon as one started to heal, the next one would erupt. I was put on valacyclovir which did a great job of stopping that. For 18 months, if I missed a day or so, the cold sores would come back. After 18 months, I just got the occasional cold sore, as I had done before getting ME/CFS. The valacyclovir solved the cold sores but didn't have any impact on my ME/CFS symptoms. I've since had another episode of constant cold sores, but this was quickly brought under control with more valacyclovir.
That's useful as an N=1 observation. I do not assume that CFS is a single disease. The metabolic and mitochondrial components might be separate from things like neurological symptoms. Maybe - in a given individual - the metabolic component has one cause, and the neurological component is a different disease - like HSV1 - that took hold because of the opportunity to exploit a low energy status in the host. It might be complicated. What are your personal neurological symptoms connected to CFS? Do they parallel general overall weakness or do the neurological symptoms have their own course and presentation separate from the body symptoms?
What is the general guideline on starting and stopping antivirals? Does that promote resistance to the drug, the way it often does with antibiotics?
I guess there is no effective way to measure viral load in the body - before and after the antiviral - because most of the virus is not in serum but resides in various tissues?
I assume that there is effectively no way to measure viral load in the brain, short of doing a spinal tap and measuring virus in cerebrospinal fluid? Obviously that is not a procedure any doctor is going to authorize in order to help treat something that medicine does not even recognize as a "disease", that was suggested in response to a research study.
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