Why one mutation can protect people from HIV

We've talked here before about the importance of the protein CCR5 in HIV/AIDS treatment research. CCR5 is a protein on the surface of immune cells. Some people have a genetic mutation, called Delta-32, which alters how that protein works, how often it appears, or changes its structure. People with the mutation have immunity to some strains of HIV, the virus that causes AIDS.

CCR5 is the key to the Berlin Patient—Timothy Ray Brown—who, until recently, was the only person to ever be cured of AIDS. Brown received bone marrow transplants from people who had the Delta-32 mutation. His body has been HIV-free for five years. And, last week, researchers announced that two other people successfully received the same treatment.

But here's the thing, until today, I didn't totally understand how the connection between CCR5, Delta-32, and HIV worked. There's a story (and some great digital illustrations) on NPR's Shots blog that makes the situation much more clear. HIV, apparently, have little spikes all over its surface. These spikes are how the virus injects itself into cells.

When it bumps into a T cell, a finger-like projection on the cell's surface, called CCR5, pushes down on the spike. This interaction pops open the HIV and releases the infectious genes into the cell. A gene therapy could protect T cells by inactivating the CCR5 gene.

Great "A-ha!" moment for me. Read the rest of the story and look at the illustrations. It'll make some thing make a lot more sense.

Read the rest at NPR's Shots blog

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  1. I wonder if the Delta-32 mutation is the same mutation that makes people immune to bubonic plague, and if the cell process is the same as with HIV.

  2. Surely, springing open the HIV cell is only half the story? You also have to open the T-cell, so that the retroviral genes get into it?

  3. Bone-marrow transplants are pretty radical treatment.  Now that we know how this works, does that mean it’d be possible to make a CCR-5 blocker drug that would help people with normal T-cells?

  4. The two new patients did not receive the Delta-32 mutation according to an NPR article.

    “Not necessarily, the Boston researchers say. The donor cells their patients got did notlack the receptor. So what’s happening with them must be different from the Berlin patient.”  Richard knox.

  5. We’ve suspected  this CCR/HIV connection for years, but blocking a chemokine receptor (CCR5 is C-C motif chemokine receptor) affects an immune cell’s ability to respond to signals.  APCs might not migrate properly or phagocytose properly in response to infection.

    You’d beat HIV and fall victim to a bacterium…Global blocking of a chemokine receptor is not good.

    1.  Hmm…any known way to temporarily turn the receptor off, wait for the HIV to flush out of the system, and then let the receptor turn back on?

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