A New Decade of ME Research: The 11th Invest in ME International ME Conference 2016
Mark Berry presents the first in a series of articles on the 11th Invest in ME International ME Conference in London ...
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Silly Questions???

Discussion in 'General ME/CFS Discussion' started by roxnhead, Apr 16, 2016.

  1. roxnhead

    roxnhead

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    Please excuse my ignorance but..... Am I contagious? I tested positive for EBV and Coxsackies B. Since it is an "active virus" is it communicable?

    Should I be washing my counters with anti-viral, bleach etc...? Should I stay away from elderly and babies, those that are immunocompromised? How diligent do I need to be around others?

    Also, How prevalent is it to have active viral EBV and Coxsackies B? Does practically everyone have it? or just those with CFS/ME? but we get ill from it.

    If I am ill because of my faulty genetics, unable to fight these viruses, are my children likely to have some of same problems since they were with me at time of my infection? It seems they are always fighting some upper respiratory infection and have mold issues.

    As always thank you for your patience. It is quite intimidating asking questions that are "ignorant". But I just don't know! The absence of knowledge is one of the the things that keeps me up at night:(! I thank you for your advice and knowledge any help is very appreciated. Be well, Roxnhead:)
     
  2. halcyon

    halcyon Senior Member

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    The short answer is that we don't really know. What we can infer from research though is that a percentage of patients with enteroviral ME do shed virion in their stool, well into the chronic phase. This means that yes, in theory, you could pass the virus you are carrying on to someone else. However, it doesn't mean that you can pass ME on to someone else. ME is a consequence of the infection. Your point about risk to your children due to genetics is possibly valid, though it's likely that if you were all around each other during the acute infection then you were all already exposed to the same virus and if they didn't develop ME from it then they are now immune to that particular serotype that you are still carrying. Also what was found in the previously mentioned research was that the virus that patients do shed is coated in antibodies and this may limit its ability to infect others.

    In light of what I said above, I don't think you need to get too intense about it. The main risk again is fecal oral contamination, so diligent handwashing and hygiene on your part is probably the most important. There is no evidence one way or another that I'm aware of looking at if we are shedding enterovirus in respiratory secretions chronically. You will be shedding EBV in your saliva but that is no different than anyone else that has it. To be safe you probably don't want to share drinks or food/utensils with the above mentioned people and wash your hands if you sneeze.

    EBV is highly prevalent (~95% of the population is infected with it) and always results in a chronic infection. Enteroviruses like coxsackie B are classically thought of as being self-limited infections that leave the body entirely upon a proper immune response within 2 months of the initial infection. There is ample evidence though showing that chronic enterovirus infections are possible and are linked to ME, chronic heart disease, chronic gastrointestinal disease, possibly T1D, muscle diseases, peripheral arterial disease, etc. To answer your question I don't think chronic enterovirus infections are highly prevalent, but they are obviously very possible. This is not well recognized by the medical field at large at this point.
     
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  3. Jonathan Edwards

    Jonathan Edwards "Gibberish"

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    Are you sure you are not just antibody positive - which just means you have met these viruses at some time in the past, as almost everybody has for EBV and a lot for Coxsackie.
     
  4. Hip

    Hip Senior Member

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    Yes, many people have these viruses, but for reasons unknown, only a small percentage with these viruses develop ME/CFS.

    Here are some prevalence rates for common pathogens:

    Epstein Barr virus is found in around 90% of adults, 1
    HHV-6 is found in nearly 100% of adults (and in 80% of children by 2 years old),
    HHV-7 is found in 98% of adults, 1
    Chlamydia pneumoniae in 74% of adults, 1
    Coxsackievirus B IgM antibodies in 23% of adults in Scotland, 1
    Coxsackievirus B3 in 7% of infants in Norway,
    Coxsackievirus B4 in 2% of infants in Norway,
    Echovirus 9 in 2% of infants in Norway, 1
    Cytomegalovirus in 58% of adults, 1
    Parvovirus B19 in 61% of adults, 1
    Herpes simplex I in 54% of adults,
    Herpes simplex II in 16% of adults. 1


    Many of these viruses are also linked to other diseases. For example, EBV is linked to multiple sclerosis. Again, it is not known why EBV might possibly be triggering MS in some people, but not in most people.

    Note that when we say a pathogen is "linked to" a disease, or "associated with" a disease, this means that statistically, the pathogen is found more commonly in those patients with the disease, compared to how common the pathogen is in the general population. But this association does not prove the pathogen causes the disease (although it's often suspected to be a possible cause).

    This may interest you: List of Human Diseases Linked To Infectious Pathogens
     
    Last edited: Apr 16, 2016
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  5. frederic83

    frederic83 Senior Member

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    The problem is not really the virus, but the non-cytolytic form of the virus. We don't know why, sometimes, a basic coxsackievirus subtype or echovirus subtype (and other virus too, although not related to CFS) evolve in this form, once it enters in the body. And this non-cytolytic virus is able the creates normal virions that can infect others people. So the risk to infect people around is higher, but we don't know if the eventual infections will progress to a non-cytolytic form, maybe the genetic is implied.
     
  6. halcyon

    halcyon Senior Member

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    Right. As I said ME itself is not contagious, but the viruses that trigger it certainly are.

    It's interesting that we do shed virus if the infection is in fact non-cytolytic because by definition this type of infection shouldn't be able to release virion. I don't believe enterovirus is able to leave intact cells via budding so it has to rely on cell lysis to shed virion.
     
  7. frederic83

    frederic83 Senior Member

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    And how a dsRNA virus inside a cell can create ssRNA virions without destroying the cell is mysterious. Any enterovirus expert here?
     
  8. Hip

    Hip Senior Member

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    There is a some understanding of why enterovirus changes into the non-cytolytic form in the body. Professors Steve Tracy and Nora Chapman and others have worked on this.

    Non-cytolytic infections only tend to form in quiescent cells (cells which are not dividing). In rapidly diving cells, few non-cytolytic enteroviruses are formed. The reason is that quiescent cells lack a factor called heterogeneous nuclear ribonucleoprotein C1 (hnRNPC1). This hnRNPC1 factor appears only during mitosis (cell division), so you don't get hnRNPC1 in quiescent cells.

    Now this hnRNPC1 factor is involved in the manufacture of enteroviral positive single stand RNA (+ssRNA).

    So in quiescent cells (which lack hnRNPC1), not enough +ssRNA is produced. Normally in lytic enterovirus infections, as the virus replicates in a cell, you get 100 times more +ssRNA produced than -ssRNA. 1

    The -ssRNA acts as a template used to create lots of +ssRNA. This -ssRNA is like photographic negative which you use to produce hundreds of photographic prints. Remember that enterovirus genome is made from +ssRNA, so to make lots of new enteroviral particles, you need to make lots of these +ssRNA photographic prints.

    But because of the lack of hnRNPC1 in quiescent cells, not enough +ssRNA is made, and thus the ratio of +ssRNA to -ssRNA goes down from around 100:1 to around 1:1. So when enterovirus tries to replicate in quiescent cells, normal replication fails, and instead of getting lots of +ssRNA photographic prints made from a few -ssRNA photographic negatives, you get equal amounts of +ssRNA and -ssRNA.

    Then because you have equal quantities, it encourages these positive and negative single strands of enteroviral RNA to join together like two sides of a zip to form lots of double stranded RNA. It is this dsRNA which is the hard-to-destroy non-cytolytic form of the virus that can live inside human cells on a long term basis.



    It's an interesting idea, though, that ME/CFS might be primary driven by a non-cytolytic enterovirus infection rather than the normal lytic enterovirus infection. In ME/CFS patients, lytic enterovirus is not always found; but you still find enteroviral RNA, which suggests there is a non-cytolytic infection going on. So this indicates the non-cytolytic side of the infection may be driving ME/CFS.

    Maybe the circumstances that determine whether ME/CFS arises after catching an enterovirus infection is whether lots of non-cytolytic viruses form. Perhaps there is something in the bodies of ME/CFS patients that favors the production of non-cytolytic enteroviruses over the production of normal lytic viruses, so that we end up with a major non-cytolytic infection. That is one speculative explanation of why ME/CFS only appears in a small percentage of people with enterovirus infections.

    These non-cytolytic enterovirus infections are also found in chronic CVB myocarditis, and type 1 diabetes.
     
    Last edited: Apr 16, 2016
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  9. halcyon

    halcyon Senior Member

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    There are several possible mechanisms that viral RNA could be using to leave infected cells without lysis, including viral synapse, autophagosomes, exosomes, etc.

    Note that what Dr. Chia has found is that in tissue samples not every infected cell contains dsRNA. In fact, the majority of infected cells in the tissue samples don't contain dsRNA. Here's a slide from one of his IiME talks:
    dsrna.png

    You can see that dsRNA is only occupying a portion of the total infected cells. Dr. Chia believes that viral persistence is achieved through dsRNA formation and that these cells are seeding infection to the surrounding tissue.
     
  10. roxnhead

    roxnhead

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    Most of my testing was done at Quest, and yes I could use some help interpreting these results:confused:


    EBV VIRAL CAPSID AG (VCA) NEGATIVE AB IGM

    EBV VIRAL CAPSID AG (VCA) 3.27 HIGH AB IGG
    (OVER 1.1 POSITIVE)
    EBV NUCLEAR AG (EBNA) AB >5.00 HIGH IGG

    COXSACKIE B 1 1.8 HIGH
    B3 1.8 HIGH
    B5 1.8 HIGH
    B6 1.16 HIGH

    So it is my understanding that these test are not valid? That I need them re-tested at a specialty lab. How much credence do I give these values? Is it worth my time, effort and money to pursue testing or spend energy on finding DR. and treatment? Will a CFS/ME specialist accept my referral without specialty lab results?
     
  11. Hip

    Hip Senior Member

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    Which lab tested you for coxsackievirus B, and what type of test was it? Do you have a link to the webpage detailing the coxsackievirus B test? Is it this webpage by any chance, which is a complement fixation test?

    Not that I know that much about it, but those titers of I:8 and 1:16 are not normally what you would class as "high".

    In fact, I:8 and 1:16 are right at the lowest end of the titer range. See this post for more details on viral titers.


    If your titers are low like yours appear to be, that shows evidence of a past infection: ie, years ago you caught these viruses, which means you are antibody positive to them; but these are not presently active infections.

    If you caught an infection in the past, you generally will have antibodies for that infection. But if the infection is not active, the antibody titer will be low.

    But anyway, complement fixation tests are often not sensitive enough to detect the chronic coxsackievirus B infections frequently found in ME/CFS patients. For a sensitive coxsackievirus B test, you would have to use ARUP Lab, which Dr John Chia uses.
     
    Last edited: Apr 19, 2016
  12. roxnhead

    roxnhead

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    So, Coxsackie B really doesnt sound like my problem. These test were run at Quest labs. What about The EBV, is this a concern? Thank you so much for your expertise and knowledge:) If I could possibly borrow your brain, just for a day or two, I promise to give it back---:D and maybe I could comprehend all this "science"!
     
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  13. halcyon

    halcyon Senior Member

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    I don't think that's the case with the Quest CF test. For me I had several that showed up as past infection on the ARUP panel that didn't register on the Quest CF test. Even my 1:640 echovirus 30 titer didn't even register on the Quest test.
     
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  14. frederic83

    frederic83 Senior Member

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    It could be just random results, because if not that means you met 4 coxsackievirus not so long ago...
     
  15. halcyon

    halcyon Senior Member

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    Yeah, that's the part that really doesn't make sense.
     
  16. frederic83

    frederic83 Senior Member

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  17. Hip

    Hip Senior Member

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    I am not sure at the moment. Normally the Quest complement fixation test (CFT) for coxsackievirus B is not sensitive enough to detect the chronic Coxsackie infections often found in ME/CFS patients.

    In other words, the CFT test may often miss Coxsackie active infections that can be present in ME/CFS patients.

    So generally speaking, the Quest test you took is pretty worthless for detecting chronic Coxsackie infections in ME/CFS patients.

    Dr John Chia, who specializes in ME/CFS linked to coxsackievirus B and echovirus, uses the ARUP Lab tests for coxsackievirus B, but unfortunately this test costs around $440.


    Did it say anything else on your Coxsackie test results document? Often just under the results there will be a sentence or two saying something like: "these results are evidence of a past, latent infection", or "these results are evidence of a current, active or reactivated infection"



    Your Epstein-Barr virus (EBV) could be a problem.

    Dr Jose Montoya considers EBV a problem in ME/CFS when EBV-EA is 1:160 or more, and an EBV-VCA IgG is 1:640 or more to be high. Reference: 1

    Your EBV-VCA IgG is 3.27 HIGH, (but I am not sure how two convert an index number like 3.27 to a titer number like 1:640).

    Basically you'd need to find an ME/CFS doctor to interpret this, but from what I can tell, EBV may well be a problem.


    You might also have a problem with coxsackievirus B, but it's hard to tell with the test that you took.
     
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  18. roxnhead

    roxnhead

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    INTERPRETIVE CRITERIA:
    <1.8 Antibody Not Detected
    > or = 1:8 Antibody Detected

    Single titers of > or = 1:32 are indicative of recent infection. Titers of 1:8 or 1:16 may be indicative of either past or recent infection, since CF antibody levels persist for only a few months. A four fold or greater increase in titer between acute and convalescent specimens confirms the diagnosis. There is considerable crossreactivity among enteroviruses; however the highest titer is usually associated with the infecting serotype.
     
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  19. Hip

    Hip Senior Member

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    I think the difficulty is the above sentence, because they are saying that for titers of 1:8 or 1:16 (which is what you have), they cannot tell whether you may have a past infection (which likely would be nothing to worry about), or a recent active infection (which may be driving your ME/CFS).

    But I am half guessing here, because I don't know enough about it.



    If you had taken the ARUP Lab neutralization tests, then the interpretation would have been more clearcut, because Dr Chia says that any titers of 1:320 or higher in the ARUP tests indicate an active infection.
     
    Last edited: Apr 20, 2016
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  20. wastwater

    wastwater Senior Member

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    Do the dsRNA and ssRNA have more of a connection to dengue fever class of pathogens
     

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