1. Guest, the 'News in Brief' for the week beginning 22nd February 2021 is here.
    Dismiss Notice
  2. Welcome! To read the Core Purpose and Values of our forum, click here.
    Dismiss Notice

Antiretrovirals

Discussion in 'Antivirals, Antibiotics and Immune Modulators' started by Hutan, Jun 11, 2018.

  1. Jonathan Edwards

    Jonathan Edwards Senior Member (Voting Rights)

    Messages:
    8,466
    Likes Received:
    89,598
    Actually @Allele, as far as I know this is not the case. I am aware that there are a number of physicians out there who claim this but the research studies have consistently failed to find any support for this. People with ME do NOT have evidence of herpesvirus reactivations in any way that would explain their symptoms.
     
  2. Allele

    Allele Senior Member (Voting Rights)

    Messages:
    1,047
    Likes Received:
    9,266

    It depends whose research you're looking at, JE.

    And in my direct experience, what you assert is not the case. Myself and nearly every patient I have ever talked to have persistent viral-like symptoms as well as high reactivation results for any combo of HSV, VZV, EBV, HHV6, CMV etc.

    This becomes very obvious when you've had HSV, bc the prodrome and outbreak have very specific presentations that are not dissimilar to the other HVs (minus the blisters.)

    These microbes are at least opportunistically activated, as in AIDS and transplants, and may be worth addressing at some point in the treatment scheme, to lessen the immune burden until we can find the cause of ME. HHV6 is known to cause encephalitis, that is not under dispute afaik. You are so quick to dismiss the actual patients who are responders to AVs.

    Dr Petersen has spent years researching HHV6, and has a lot of evidence that aligns with and confirms a significant subset of patient experience. Montoya and Lerner also found a subset of responders. Van Elzakker has a working hypothesis as well.

    This issue has been neither proven nor disproven in a definitive way.

    So it depends on which research studies your'e looking at. You have your theory, supported by your chosen evidence, I have my direct experience, supported by another set of studies.

    There is a conundrum in insisting that something has to be definitively proven by a science that has not yet definitively proven something. I don't have that luxury, and from my vantage that's an absurd logical feedback loop.

    https://hhv-6foundation.org/associated-conditions/hhv-6-and-chronic-fatigue-syndrome
     
    MEMarge, merylg, duncan and 2 others like this.
  3. Jonathan Edwards

    Jonathan Edwards Senior Member (Voting Rights)

    Messages:
    8,466
    Likes Received:
    89,598
    I am looking at published studies, including those of Dr Peterson. In fact I do not have a theory so I am not choosing evidence, just looking at it. I have gone through Dr Peterson's publications. Two seem relevant. In a study of patients with neurological symptoms he found evidence of HHV6 in 2% - not that many. It seemed to be more than control levels but the study looks to be retrospective, specialist referral centre based and not using blinded controls so I am not sure one can make much of it. The other study of some clusters of CFS patients says that there was no evidence for involvement of HHV6. So what am I missing? Why has nobody been able to find substantive evidence for involvement of HHV6 in CFS, including it seems Dr Peterson himself?
     
  4. Allele

    Allele Senior Member (Voting Rights)

    Messages:
    1,047
    Likes Received:
    9,266
    [post deleted by me due to editing by mod team]
     
    Last edited: Jun 17, 2018
    ScottTriGuy, duncan and Inara like this.
  5. Jonathan Edwards

    Jonathan Edwards Senior Member (Voting Rights)

    Messages:
    8,466
    Likes Received:
    89,598
    I think what I am saying is that it is not just incomplete but pretty much zero. Anything is possible but one has to have some level of consistency to follow a particular line of thinking.
     
  6. Inara

    Inara Senior Member (Voting Rights)

    Messages:
    2,714
    Likes Received:
    11,088
    But there's the statement by Lipkin: 85% of Montoya's cohort showed retrovirals signs (my layman words). Well, it is said to have been said by him...Since it wasn't followed, was it later decided this finding has no relevance? And what were the reasons?

    There was also a statement that XMRV has biological safety level 2. Is that old? Why was that? Was that a consequence of the XMRV findings then, and now that changed?

    I can only speak for myself: I don't take any side. I want to try to understand as much as possible with my little knowledge in this field.
     
    MEMarge, merylg, sb4 and 2 others like this.
  7. Inara

    Inara Senior Member (Voting Rights)

    Messages:
    2,714
    Likes Received:
    11,088
    Two family members who have ME have virus reactivation (at least Zoster and Simplex) which is pretty obvious due to clinical presentation. I guess they have an immune deficiency but they cannot check (because they can't travel). I had "only" slightly low IGG3 but this was enough to have every 1-2 months bad infections, and I don't mean a bit of a snuffy nose. Sometimes it seemed I didn't have to have had contact to others - and again, an infection.

    It is typical for ME to have crashs/PEM/PENE after an infection. In my experience, those infections were a downward path that led to a slow and constant worsening of the status. My impression from just my personal experience in my family is that infections contribute substantially.

    On the other hand, I have heard of several people with ME who didn't have an infection in years. So there is something different.
     
    merylg likes this.
  8. Allele

    Allele Senior Member (Voting Rights)

    Messages:
    1,047
    Likes Received:
    9,266
    Yes, that's exactly it. It is simply within the specific context of a study that shows zero, that it is zero for the parameters of that study: the thing looked for, the place(s) it was looked for, and the tools, means and methods that were used. That does not rule out that different, perhaps yet to be discovered or utilised means, methods, tissues examined etc will also show zero.

    I'm not attached to virus, autoimmune, whatever; I just remain open to the reality that our thinking (when confined to its acquired knowledge base) is inherently limited by its existing datasets, which are by nature never complete.
     
    MEMarge, merylg, Hutan and 4 others like this.
  9. duncan

    duncan Senior Member (Voting Rights)

    Messages:
    940
    Likes Received:
    3,668
    A confounding factor may be that pre-existing dogma, regardless of its pedigree, may be flawed or even corrupted.
     
    merylg, Inara and Allele like this.
  10. Samuel

    Samuel Senior Member (Voting Rights)

    Messages:
    381
    Likes Received:
    1,946
    > People with ME do NOT have evidence of herpesvirus reactivations in any way that would explain their symptoms.

    i'm possibly too fogged to comment responsibly, but:

    anecdotally, these show up occasionally in pwme. mary, for example, mentioning ablashi, seems to say it can be worth doing something about it, as a factor that can improve, but not cure you.

    are you strictly talking about causation per se? or are you addressing these cases?

    in my case, i have the following:

    hhv 6 igg antibodies
    9.6 /high/ >.99 is positive
    [despite the fact that i seem to be immunocompromised]

    but human herpes virus type 6 igm neg

    adn i haven't the slightest clue whether it's worth doing something about it.
     
    Inara likes this.
  11. Jonathan Edwards

    Jonathan Edwards Senior Member (Voting Rights)

    Messages:
    8,466
    Likes Received:
    89,598
    When I heard Lipkin presenting these data he was very clear that there was no reason to think these retroviral signals meant anything. I presume he was using PCR so a positive would men that somewhere in a sample there was at least one piece of DNA that looked like a retroviral sequence.

    I think this should probably be compared to mycobacteria. We are concerned if someone with pneumonia has mycobacterium tuberculosis in their spit but we probably all have mycobacterial DNA on our fingers and in our spit all the time because mycobacteria are a major constituent of soil. Bacteria, viruses, retroviruses, plasmids etc. are everywhere, especially if you look using hugely powerful amplification methods.

    I do not remember Lipkin commenting specifically in relation to the retroviruses but he made the general statement that if anything there were more viruses in healthy samples and nothing came out as more common in ME. That means there is no reason to follow anything up.

    I cannot see that it makes any sense at all to suggest that Lipkin spent all this time looking for viruses and then ignored a possible relevant finding. His lab is quite clearly hoping it will find a pathogen, otherwise why waste years looking?
     
  12. Jonathan Edwards

    Jonathan Edwards Senior Member (Voting Rights)

    Messages:
    8,466
    Likes Received:
    89,598
    The reality is that you cannot draw any conclusions from this sort of thing. Reactivation of HSV is very common. Zoster is common enough. There is no need to suggest immunodeficiency - except perhaps in a young child or if the zoster is bilateral or widespread. A slightly low IgG3 is very unlikely to be relevant to infections. Unfortunately there has grown up a mythology that people with ME are immunodeficient. But when labs have recently tried to repeat the findings they have found nothing consistent. Again, recently, a good immunology lab has found no evidence of anything wrong with NK cells. As of now my reading of all the available literature is that we have no reliable evidence for immunodeficiency in ME. That is why I was rather annoyed that in Jen Brea's film Nancy Klimas still gives the impression that there is some gross immune abnormality. I spent my life working in clinical immunology. There is nothing that convinces me we can find any clinically relevant immunological difference in PWME.
     
  13. Jonathan Edwards

    Jonathan Edwards Senior Member (Voting Rights)

    Messages:
    8,466
    Likes Received:
    89,598
    No, no need. The results show that you have encountered HHV6 in the past and have good levels of antibody immunity. Very satisfactory.
     
  14. Inara

    Inara Senior Member (Voting Rights)

    Messages:
    2,714
    Likes Received:
    11,088
    Do you have more information? Would it be sensible to have a "screening" for viruses or bacetria? (For parasites one should also look, I think.)

    I remember @Jonathan Edwards saying again and again that those titers (I hope I recollect correctly - please do correct me if not) aren't reliable, e.g. that a high titer doesn't necessarily mean problems with viruses/bacteria. I then wonder: How do virus/bacteria scientists know to interpret their results correctly, because all they get are those titers or - in the best cases - pictures or antibodies to viruses/bacteria? If that doesn't mean anything how can we trust any findings? At and last, how can we trust HIV does exist?! Maybe all these HIV deniers are right after all. (This is provocative I know, but it would be a possible consequence.) Maybe it's about beliefs and intuitions? If deFreitas' findings are false (someone linked to http://www.ncf-net.org/forum/revelations.html, I had read Osler's Web), if Mikovits', Coffins', Lipkin's&Montoya's and others' findings are false - who mainly did qualitative research then I would say - why were Gallo and Montagnier, using much older techniques than we have today? Because they found it independently from each other?

    What's interesting: DeFreitas' didn't get any grants to continue her research about her previous findings in ME, and nobody was interested. Again I ask why. Is it so obvious that this direction is bullshit? If yes, there must be so easy explanations even I can understand and accept as correct. Or was there a "tiredness" of retroviruses, "oh God, not again that crap"?

    Another thing that got me thinking is my own family history. I was told my grand-grand-grandfather had the disease I and other family members have, too. He probably was born somewhere around mid 19th century - no retroviruses from vaccines etc then. But probably other retroviruses? Do we know anything about diseases due to retroviruses in the farther past?

    It's possible the disease in my family isn't ME. It's also possible that any virus, bacterium or parasite can cause/start ME, and the susceptibility to ME is genetic. I can also think of so many other plausible explanations, including prions or metabolic stuff, channelopathies. I sometimes think ME is the symptom presentation of many different causes we still have to find.
     
    merylg and Samuel like this.
  15. Inara

    Inara Senior Member (Voting Rights)

    Messages:
    2,714
    Likes Received:
    11,088
    No you cannot. But at least in maths one counter example is enough to show the claim is false.

    I have heard now several people here telling of virus problems. So there are several counterexamples.

    If a person has shingles several times a year or even constantly for months, that's not normal.

    I hear more often that a slightly lower Igg3 (or Igg1 or Igg2) level is unimportant. Immunologists don't tend to say that in my (small) experience. I would wish those people could falsify that via experiment. If you have a job and you miss every 1-2 months for at least 2 weeks you'd be fired pretty fast. And finding a new job will be pretty hard. If you work despite the infection that could lead to serious problems. Besides the fact that you can't live a normal life if your sick that often. At least in my case, the infections disappeared with giving Igg and I am thankful someone dudn't dismiss my symptoms so fast.

    Normal ranges don't make reality, reality makes reality. I never understood why "normal ranges" dictate everything. If a treatment could help (which needs to be estimated), why is it not tried?

    The reality is also that in trials, the selection criteria are mostly questionable. I am sometimes not so sure if the disease described by Peterson, Ramsay&Co is the same that we are talking about right now. Maybe it doesn't exist anymore. (That doesn't implicate the disease that I and others have is irrevelant. It just means things could be mixed up.) By the way, when reading posts from 2012, this was discussed up and down, too, so regarding selection criteria nothing has changed. I think this is a huge problem. Because in fact, we can't draw conclusions from findings.
     
    merylg and Samuel like this.
  16. Trish

    Trish Moderator Staff Member

    Messages:
    30,717
    Likes Received:
    146,373
    Location:
    UK
    But Pure Maths and Science are fundamentally different. In Maths, you start from a set of axioms and make deductions of things that follow from those axioms, so you can 'prove' something is true for those axioms.

    In science, you make observations, and use those to make a theoretical model that enables you to hypothesise what might happen in particular circumstances.

    But, particularly in biology, we can never set the circumstances exactly as our model specifies, so we have to test the hypothesis many times and work out probabilities that the hypothesis is correct. A few 'counterexamples' don't automatically disprove the hypothesis.

    For example, when a drug is tested and shown to be effective in most cases, some of the patients won't recover, because their particular biology includes factors that prevent that drug working in their cases. That doesn't disprove the hypothesis that the drug is useful for that condition.

    Similarly, if a few people try an 'untested' treatment for a particular condition and their health improves, that doesn't prove the drug is effective for that condition. It may equally be that that person's health was going to improve anyway. That's why we need large double blind trials to find out whether the drug effect is likely to be a result of the drug, not chance fluctuations.

    I'm not sure whether this addresses the point you were making...
     
  17. Jonathan Edwards

    Jonathan Edwards Senior Member (Voting Rights)

    Messages:
    8,466
    Likes Received:
    89,598
    The answer to that is simple. Virologists draw conclusions from paired samples a fortnight apart at the time of an illness that show a major increase in titre level. They can also grow the virus in cell culture or image it by electron microscopy or find DNA. The problem in the ME world has been when physicians have used single titres as if they meant something just by being high - or repeated high titres over time. Virologists do not do that generally speaking.
     
  18. Inara

    Inara Senior Member (Voting Rights)

    Messages:
    2,714
    Likes Received:
    11,088
    yes I know :)

    still I think examples shouldn't be dismissed too fast.
     
    Subtropical Island and Trish like this.
  19. Inara

    Inara Senior Member (Voting Rights)

    Messages:
    2,714
    Likes Received:
    11,088
    I don't understand that completely. Can you explain in more detail?
     
  20. lansbergen

    lansbergen Senior Member (Voting Rights)

    Messages:
    616
    Likes Received:
    2,249
    It is as simple as he says. Draw blood, wait two to three weeks and draw again, Then compare titres.
     

Share This Page