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Medicine

Researchers Block HIV Infection In Monkeys With Artificial Protein 96

An anonymous reader writes: Immunologists have developed a synthetic molecule that's able to attach to HIV and prevent it from interacting with healthy cells. "HIV infects white blood cells by sequentially attaching to two receptors on their surfaces. First, HIV's own surface protein, gp120, docks on the cell's CD4 receptor. This attachment twists gp120 such that it exposes a region on the virus that can attach to the second cellular receptor, CCR5. The new construct combines a piece of CD4 with a smidgen of CCR5 and attaches both receptors to a piece of an antibody. In essence, the AIDS virus locks onto the construct, dubbed eCD4-Ig, as though it were attaching to a cell and thus is neutralized." The new compound was tested in monkeys. After successively higher injections of HIV, all four monkeys who received the compound beforehand stayed from free infection. Any potential medical treatment is still a ways off — the researchers plan more trials in monkeys before involving humans in the testing.
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Researchers Block HIV Infection In Monkeys With Artificial Protein

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  • by seven of five ( 578993 ) on Wednesday February 18, 2015 @12:58PM (#49080477)
    You've no idea what a pain it is to get a monkey to use a condom.
    • by Anonymous Coward

      You've no idea what a pain it is to get a monkey to use a condom.

      Why do you say that? Do they go Ape when you ask or something?

    • And here I was thinking the study had been conducted in the halls of congress; now I can not get the picture of a primate in the halls of congress walking around with a condom on.
  • Very soon we will completely cure AIDS and Cancer in monkeys.
    • This technique will likely be effective against virons in blood plasma, but it will do precisely nothing to a quiescent provirus, so an infected individual will retain infection reservoirs. Unless the active protein can cross the blood-brain barrier, brain infection will also continue and will still lead to accelerated cognitive decline and aids-related dementia. Assuming that it works, this is a godsend for effective control, but a cure it likely is not. A cure will only be accomplished when the silent res
      • You're correct that this doesn't sound like a cure. On the other hand, it might be both a very effective vaccine for the uninfected, and a reliable treatment for those infected. (This depends mostly on HIV's ability to mutate these receptors into something that can reject the drug but still connect to the target cells.) Even if a vaccine isn't a cure, it can lead to eradication of the disease. The smallpox vaccine wasn't a cure either, for example, but with sufficient coverage it was quite effective.

      • If you can cause the protein to be generated in the blood, why not also treat cells on the brain side of the blood-brain barrier as well to produce the protein and so protect the brain?

        If you can do that, you can halt transmission to new people, and halt progression of the disease on both sides of the blood-brain barrier, it's about as close to a cure as could be achieved without actually destroying all the quiescent viruses.

        Heck, it might actually cause less damage to the host than destroying all the quies

  • by Mortiss ( 812218 ) on Wednesday February 18, 2015 @01:15PM (#49080603)
    This type of compounds (HIV fusion inhibitors) is already well known and available on the market e.g. Enfuvirtide [wikipedia.org]

    The only hope here is that this inhibitor will be cheaper and perform better in humans than already available ones. However, according to FA, these type of experiments are still way off..
  • My understanding of HIV is that when it infects human cells, it hijacks the tRNA (iirc) so that the human cells continue producing more HIV viruses. With the article describing synthetic antibodies binding to HIV, the virus is unable to infect human cells. So this would seem like a race condition where the antibody needs to get to the HIV *before* HIV has a chance to infect a human cell. How can this happen reliably?
    • You'd just have to stay on the treatment until all of your already infected cells die.
    • My understanding of HIV is that when it infects human cells, it hijacks the tRNA (iirc) so that the human cells continue producing more HIV viruses. With the article describing synthetic antibodies binding to HIV, the virus is unable to infect human cells. So this would seem like a race condition where the antibody needs to get to the HIV *before* HIV has a chance to infect a human cell. How can this happen reliably?

      Mostly through concentration: making sure there are 100x or more antibodies against HIV present than the cells HIV is targeting.
      But it's also helped by binding affinity. When a receptor and a substrate bind, it's generally reversible -- they can join or separate, and there is a measurable equilibrium between the bound and unbound states, which is a function of concentration of both receptor and substrate, and a constant that reflects how well they actually stick together. Generally, antibodies are _vastly

  • I can understand Freeing a Stayed Infection, or even Staying Infection from Freedom. But what the heck is this?
  • I'm amazed that TFS says HIV as well as the first link. TFNA (The Fucking Nature Article) title is "AAV-expressed eCD4-Ig provides durable protection from multiple SHIV challenges". Wow, SHIV is right there in the title. Humans can be infected with "human immunodeficiency virus". Simians can be infected with "simian immunodeficiency virus".

    Additionally, plenty of "monkeys" get SIV and don't become symptomatic because they're natural hosts. Rhesus macaques (as stated in the Nature article), however, a
  • all four monkeys who received the compound beforehand stayed from free infection

    "Come for the injection, stay from free infection!!"

  • We already have drugs that work pretty much the same way. This is just another of the same sort that can go in our toolchest.

    But we really need a vaccine.

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