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Two existing blood pressure drugs shown to inhibit coxsackievirus B

Discussion in 'Antivirals, Antibiotics and Immune Modulators' started by Hip, Oct 5, 2011.

  1. Hip

    Hip Senior Member

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    Two existing blood pressure drugs shown to significantly inhibit coxsackievirus B

    Two existing blood pressure drugs, bosentan and valsartan, have been shown to significantly inhibit coxsackievirus B in vitro:

    Antiviral effect of Bosentan and Valsartan during coxsackievirus B3 infection of human endothelial cells.

    So I am thinking these drugs might be very useful for those with enterovirus-associated CFS.

    The antiviral action of these two drugs is mediated by their action of lowering the number of coxsackie-adenovirus receptors (CAR) expressed on the cellular surface. Coxsackievirus B uses the CAR receptor to enter the cell; so with reduced CAR numbers, the infection is also reduced.

    The study found that the viral load in drug-treated cells was significantly lower for both bosentan and valsartan, as much as a 5-fold and 10-fold reduction respectively.

    Valsartan looks easier to use than bosentan, as bosentan use requires regular liver function checks by your doctor when you use it. And valsartan seems to have more potent antiviral effects.

    Any unwanted blood pressure lowering effects from these drugs might be counteracted by simultaneously taking blood pressure raising supplements like licorice, ginseng, or salt. Drinking more water can also raise blood pressure.

    Note that the above study was performed in vitro, not in vivo, so these antiviral actions may not necessary pan out in patients.

    However, the tenfold reduction in viral load obtained from valsartan is pretty impressive, and if this does pan out in vivo, this might be very beneficial to those with enterovirus-associated CFS.

    The cells targeted by the drugs are:

    Epithelial cells which make up the lining of the mucous membranes of the whole respiratory-gastrointestinal tract (and the lining of serous membranes too).
    Endothelial cells which make up the lining of blood vessels.

    Epithelial cells are, I believe, a major reservoir for coxsackievirus B infection, so these drugs would appear to hit this virus right in its home territory.
     
  2. CBS

    CBS Senior Member

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    Western US
    Thanks for the post. Interesting and would definitely provide relief to many if the in vivo testing works out.
     
  3. Hip

    Hip Senior Member

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  4. Hip

    Hip Senior Member

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    One problem with this approach, I have just found, is that if you reduce CAR expression to fight coxsackievirus B infection (the CAR receptor being the means by which coxsackievirus B enters human cells), then it seems that in long term chronic coxsackievirus B infections, this virus can soon evolve into variants that are capable of CAR-independent viral entry into cells.

    Reference: Virus Host Co-Evolution in a Persistent Coxsackievirus B3 Infected Cardiomyocyte Cell Line

    Cunning buggers, these Coxsackie B viruses.

    In chronic infections, it seems you get this virus / host co-evolutionary battle. The pace of evolution is fast in RNA viruses like coxsackievirus B, as there is a higher error rate in RNA duplication, thus always leading to many genetic variation of the virus constantly emerging within the host ideal circumstances for rapid and flexible viral evolution.
     

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