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Anyone Treating the Eight Herpes Viruses with Antivirals?

Discussion in 'Infections: Lyme, Candida, EBV ...' started by pone, Sep 21, 2019.

  1. pone

    pone Established Member

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    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.

    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.
     
    Last edited: Sep 23, 2019
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  2. beverlyhills

    beverlyhills Established Member (Voting Rights)

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    This has not been completed in a research capacity, let alone a clinical one.

    Yes, you measure quantitative PCR copies of CMV/EBV in the cerebrospinal fluid or you do post-mortem in situ hybridization, it's pretty easy and make sure it regiospecific for the susceptible substructures.






     
    Last edited: Sep 25, 2019
  3. beverlyhills

    beverlyhills Established Member (Voting Rights)

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    2009: Epstein-Barr virus infection is not a characteristic feature of multiple sclerosis brain.
    2018: Epstein-Barr virus is present in the brain of most cases of multiple sclerosis and may engage more than just B cells


    If you want to read both those studies, they are pretty in-depth. CFS research is at the pre-2009 stage.
     
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  4. pone

    pone Established Member

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    As a patient, I would not be crazy about the post-mortem solution :)

    Just for hypothesis sake, if I had an HSV1 chronic low-level infection of the cerebral cortex, would the viral load in CSF parallel in some way the viral load in the relevant brain tissue? I would hope yes since the body is cleaning out some of the virus on an ongoing basis, and that gets washed into the CSF.
     
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  5. duncan

    duncan Senior Member (Voting Rights)

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    @pone , I would be interested in pursuing this cortex atrophy possibility a little further. Do you have any references you can provide a link to? If so, many thanks in advance.
     
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  6. pone

    pone Established Member

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    Read the master post and look for the link to the Taiwan study, which is causing big waves in Alzheimer's circles. This study did not establish tight causality, but the associations seem pretty obviously destined to be proven out as causalities. The study shows that:

    1) If you have HSV1 over age 50, your 10 year risk of Alzheimer's raises 250%.
    2) If you treat the HSV1 with antivirals, the Alzheimer's risk vanishes.

    Atrophy goes with Alzheimer's, and the typical Alzheimer's patient is losing cortical mass steadily over decades leading up to the diagnosis.
     
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  7. beverlyhills

    beverlyhills Established Member (Voting Rights)

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    Yes, but HSV is pretty hard-pressed to cause post-viral fatigue since it rarely mimicks CFS symptoms even during acute induction, and focuses more on peripheral ganglion.

    The load does not really matter though. People can be allergic to herpesviruses like they can bananas, and it causes a mechanical destruction of neurons. Researchers are focusing on molecular interactions of post-viral fatigue, but it is only a chemical process in the way that a car crash is.

    Studies on plasma are like investigating the air inside of the car during the catastrophic event while the corresponding frame is being destroyed.
     
  8. wastwater

    wastwater Senior Member (Voting Rights)

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    EBV still seems to be of high interest to the MS St Barts blog
    A basic fact I never see mentioned is EBV surpresses FOXO1 And I think that’s important
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1642148/
    FOXO1 controls many pathways

    Could you have EBV that leads to insulin resistance
     
    Last edited: Oct 12, 2019

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