1. Standard memberPalynka
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    13 Nov '08 18:24
    http://online.wsj.com/article/SB122602394113507555.html

    It's just a single case, so there's much more work to be done. Still, it sounds promising.
  2. Subscribersonhouse
    Fast and Curious
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    13 Nov '08 19:00
    Originally posted by Palynka
    http://online.wsj.com/article/SB122602394113507555.html

    It's just a single case, so there's much more work to be done. Still, it sounds promising.
    Hear is another approach that might work:
    Genetically engineering the immune cells. The potential problem with this approach is it might be a bit TOO powerful and go on to attack human cells ala Auto-immune diseases but if they can avoid that, they might be on to something here.
    http://www.newscientist.com/article/dn15156-pimped-up-tcells-seek-out-and-destroy-hiv.html
  3. Joined
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    14 Nov '08 15:45
    The main problem with attacking HIV is that some of its virus hide themselves in the CNS while the others are attacked.

    I think the hardest part should be comletely eradicating this from the body, because it tends to reappear once the virus finds the environment less hostile towards itself.
  4. Standard memberPalynka
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    14 Nov '08 16:03
    Originally posted by dannyUchiha
    The main problem with attacking HIV is that some of its virus hide themselves in the CNS while the others are attacked.

    I think the hardest part should be comletely eradicating this from the body, because it tends to reappear once the virus finds the environment less hostile towards itself.
    But did you read about the genetic mutation involved? When this mutation is present, the virus cannot enter cells.
  5. Standard memberyo its me
    watch the acid...
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    15 Nov '08 09:41
    Amaising what science can do. Can someone put this possiable cure on billboards accross south Africa more then the HIV sufferes might be saved.
  6. SubscriberAThousandYoung
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    15 Nov '08 23:09
    Originally posted by Palynka
    http://online.wsj.com/article/SB122602394113507555.html

    It's just a single case, so there's much more work to be done. Still, it sounds promising.
    Wow.

    I used to be a volunteer massage therapist at an AIDS patient center in north Oakland. One of my clients talked about how he had unprotected sex with his boyfriend because the boyfriend was "of pure Aryan stock and therefore immune".

    Maybe there was something behind that ridiculous story after all.

    The mutation prevents a molecule called CCR5 from appearing on the surface of cells. CCR5 acts as a kind of door for the virus. Since most HIV strains must bind to CCR5 to enter cells, the mutation bars the virus from entering. A new AIDS drug, Selzentry, made by Pfizer Inc., doesn't attack HIV itself but works by blocking CCR5.

    About 1% of Europeans, and even more in northern Europe, inherit the CCR5 mutation from both parents. People of African, Asian and South American descent almost never carry it.

    http://online.wsj.com/article/SB122602394113507555.html
  7. Joined
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    16 Nov '08 13:34
    Originally posted by AThousandYoung
    Wow.

    I used to be a volunteer massage therapist at an AIDS patient center in north Oakland. One of my clients talked about how he had unprotected sex with his boyfriend because the boyfriend was "of pure Aryan stock and therefore immune".

    Maybe there was something behind that ridiculous story after all.

    The mutation prevents a molecule ca ...[text shortened]... descent almost never carry it.

    http://online.wsj.com/article/SB122602394113507555.html
    The CCR5 delta 32 (D32) mutation has been known for well over a decade now.
    See original paper Dragic et al. HIV-1 entry into CD4+ cells is mediated by the chemokine receptor CC-CKR-5. Nature. 1996 Jun 20;381(6584):667-73.
    http://www.ncbi.nlm.nih.gov/pubmed/8649512?ordinalpos=20&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

    CCR5 D32 is actually absent from native African, American Indian, and East Asian ethnic groups. The mutation is found principally in Europe and western Asia, with higher frequencies generally in the north. Homozygous carriers of the D32 mutation are resistant to HIV-1 infection because the mutation prevents functional expression of the CCR5 chemokine receptor normally used by HIV-1 to enter CD4+ T cells. HIV has emerged only recently, but population genetic data strongly suggest D32 has been under intense selection for much of its evolutionary history. Much work is going into designing drugs to "phenocopy" the CCR5 D32 mutation by antagonising normal receptor function. I think the radiation treatment is the key but the mortality rate of one-third is pretty grim and I think if I live in the west I would keep taking the HAART drugs. Very interesting stuff. Other resistance alleles to HIV-1 in humans are known, such as CCR2-64I and SDF1-3'A.
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