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Ibalizumab: monoclonal antibody for HIV. Maybe for ME?

Discussion in 'General ME/CFS News' started by ScottTriGuy, Jun 13, 2016.

  1. ScottTriGuy

    ScottTriGuy Stop the harm. Start the research and treatment.

    Toronto, Canada
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  2. Justin30

    Justin30 Senior Member

    Wow good news.
  3. Kati

    Kati Patient in training

    Hi @ScottTriGuy by definition, monoclonal antibodies are targetted drug therapies. There is an increasing number of monoclonal antibody drugs one the market these days, each one of them targetting different cells or systems.
    For instance, Rituximab which is one of the first generation of Mab, targets the B-cells.

    Here is what wiki says about Ibalizumab:
    Ibalizumab (TMB-355[1] previously known as TNX-355) is a non-immunosuppressive monoclonal antibody that binds CD4, the primary receptor for HIV, and inhibits the viral entry process.[2] It is being investigated as an HIV entry inhibitor[3] with the ability to block both CCR5- and CXCR4-tropic viruses,[4] and is undergoing a Phase II clinical trial with an estimated study completion date in December 2010.[5] Specific Research is also conducted at the Aaron Diamond AIDS Research Centerunder the direction of David Ho.[6][7]

    I would be very surprised that this drug would have any effect on us. We have no good reasons to believe any retrovirus is implicated at the moment.

    I am hoping that research from different teams will stimulate drug development, including monoclonal antibodies should diverse antibodies circulate in our patient population (muscarinic, adrenergic, etc)

    As always, more research is needed.
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  4. Justin30

    Justin30 Senior Member

    cell-associated virus levels were also reduced in the blood, lymph nodes and the gut.
  5. Snow Leopard

    Snow Leopard Hibernating

    South Australia
    This drug will hopefully be found effective for treating HIV!

    But it is highly specific for treating that virus - it won't treat other retroviruses, nor ME.
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  6. Marky90

    Marky90 Science breeds knowledge, opinion breeds ignorance

    I agree

    Since it is the CD4-glycoprotein that is targeted, and not the cells with CD4 on, it seems unlikely that anyone with ME would have benefited. A very concrete mab!
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  7. alex3619

    alex3619 Senior Member

    Logan, Queensland, Australia
    There could be some cross-reactivity of antigens with antibodies, but this occurs with decreased effect. Antibodies are like complex locks, looking for the key that fits them. They are very specific to a very specific key. Kind of similar keys might kind of work though. However its likely that our own antibody production would do so better by random chance than any HIV specific antibody would. Since we are not all being cured by this all the time (though I might pose some caveats to that line of thinking) its highly unlikely it will help.

    Having said that there appears to be a rare subgroup of HIV patients who have something ME-like. We know this because of one un-named patient who has a bad showing on the two day CPET. So there might be people with undiagnosed HIV who might benefit. However, and this is my experience, when I mention my symptoms to a new doc, or at a hospital, one of the first things they get me tested for is HIV (and most recently also for blood alcohol, which is kind of a joke). I have been tested for HIV so very many times. What are the odds all of those tests are false negatives? How is it that, even with probably decreased lifespans, we are not rapidly dying with HIV? Its very very unlikely any such drug would help.

    Here is what might bring it home. When a virus mutates even a little, a therapeutic antibody might fail. Indeed this is how viruses, like HIV, evade the immune system, at least in part. You develop an antibody, one or several nucleotides mutate in the virus, and then the body no longer has a useful antibody. Yet the human immune system has a huge variation of antibodies available to it. Any synthetic antibody is very limited into what it binds to.

    What we might be able to do, theoretical so far I think, is clone our immune cells in vitro, introduce the pathogens, then note the immune response. Yet to duplicate the complex interacting factors found in immune cells inside the body might be a very difficult task.
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