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Injecting coxsackievirus B infected mice with DAF and CAR receptors stopped the virus

Discussion in 'Other Health News and Research' started by Hip, Jan 20, 2012.

  1. Hip

    Hip Senior Member

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    In the studies quoted below, recombinant (= artificially synthesized) DAF and CAR receptors were experimentally injected into mice that had coxsackievirus B infections. DAF and CAR are receptors are normally located on the surface of the cell, and coxsackievirus B latches onto these receptors in order to break into and infect a cell.

    It would appear that by injecting these artificial, recombinant DAF and CAR receptors into the mice, the coxsackieviruses attached to the recombinant DAF and CAR receptors instead, rather than the real DAF and CAR receptors on the mice's cells. Doing this blocked the coxsackievirus infection.

    This might translate to a chronic fatigue syndrome treatment option in the future, as of course ME/CFS is strongly linked to chronic coxsackievirus B infection. It looks promising.


     
    Last edited: Apr 12, 2014
  2. alex3619

    alex3619 Senior Member

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    Hi Hip, this approach will work with ANY virus. It has one drawback though. The receptor-virus combination can be seen by the immune system. If an antibody based immune response is launched, there is a risk of an autoimmune attack on those receptors. Now for acute life-threatening viral attack, the risk is probably worth it. For a chronic viral infection the risk is probably not worth it.

    There is another approach that is similar but I don't have a reference handy. They could put the receptors in a filter and pass the blood through it, similar to dialysis.

    Bye, Alex
     
  3. Hip

    Hip Senior Member

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    Very interesting point, Alex. Is an autoimmune attack on the receptors a known and observed risk of such a therapy, or this a theoretical concern, as far as you know? I can certainly imagine it could be a problem.
     
  4. alex3619

    alex3619 Senior Member

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    Hi Hip, its a theoretical concern, but well grounded. It is why molecular mimicry is such an issue with pathogens. An antibody binds to a particular shape of molecule (where shape includes things like charges and not just physical shape). If a receptor binds to a virus, then the immune system could flag the virus-receptor complex as a target. The immune system will look for a match. Under those circumstances it might accidentally lock onto the receptor part (and hence induce autoimmunity), or an overlap between receptor and virus (which is less worrying). Bye, Alex
     
  5. Hip

    Hip Senior Member

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    I wonder if this is the cause of many types of autoimmunity in general. In ME/CFS, 50% of patients have antibodies to the acetylcholine muscarinic receptor (ref: here).

    The acetylcholine muscarinic receptor is found on the parasympathetic ("rest and digest") nervous system, and these muscarinic receptor antibodies are likely causing some parasympathetic dysfunction and dysautonomia.

    But what I'd like to know is how the immune system comes to make the mistake of creating antibodies against the muscarinic receptor. Might it be a similar thing to what you have described, where a receptor somehow gets attached to a viral particle?
     
  6. alex3619

    alex3619 Senior Member

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    Hi Hip, thats one theory. The other is basically a mistaken identity theory. Something toxic in the blood, or just seems to be toxic, has a simlar amino acid configuration to, for example, the acetylcholine receptor. So the body makes antibodies to the first substance, but then they have an effect on the recptor (though perhaps a weaker effect as its only a similar molecule, not quite the same). This is the thought behing mimicry: some pathogens deliberately make proteins similar to ones in the body. If the body mounts an immune defence, it also attacks itself, weakening itself so the pathogen has a better chance of survival. Bye, Alex
     

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