reply to post by Sinny
I was urged to post a reply to this thread because I work with the lab that published this data, although I work on other anti-HIV genes/genetics
manipulations of "stem cells" in hopes of an engineered cure for HIV disease. Hopefully, it doesn’t turn into a dissertation.
First, and the most obvious question for scientists, how does this specific treatment engineered to make super killer T cells get around the fact that
T cells are killed by HIV? This is actually not a trivial question. While everyone knows that HIV preferentially infects CD4-expressing cells (CD4
is a protein on the surface of T cells and macrophages), all T cells begin as CD4-expressing cells in the thymus as they develop. And as such,
thymocytes (young and immature T cells) are exquisitely sensitive to HIV. This is part of the reason HIV infected individuals cannot recover their
CD4 T cell compartment and succumb to AIDS. Honestly, it is such a valid point, that even most (dare I say all) of the researchers involved in this
study didn't think it would work. But we continue for a number of reasons:
(1) We never expected gene therapy approaches towards HIV would work with one candidate anti-HIV gene. Yes, because the virus mutates at rates faster
than you can barely comprehend! That's why we are working full speed on half a dozen other anti-HV gene therapy candidates. We hope that as we
determine which anti-HIV candidates work individually, we can begin to create combinations containing more than one anti-HIV gene in hopes of
combating the high mutation rate. We have been working closely with mathematicians who have modeled that depending on specifically how we inhibit the
virus, we will likely only need two or three anti-HIV genes.
(2) These are cutting edge, never been done before, "proof of principle studies." Let me expound on this topic and hopefully answer another's
question in the process...
Remember I said HIV preferentially infects CD4 T cells? These are the helper T cells someone posted about earlier. Meanwhile, the killer T cells,
once they are mature, don’t express CD4 anymore (making them now unable to be infected be HIV) and now express the marker CD8 – so we call them
CD8 killer or cytotoxic T cells. These cells have a very cool, very, very, very, very, very, very specific protein that enables them to attack only
one specific target. So, for example when you get the flu, you generate CD8 cytotoxic T cells that can specifically recognize the flu, but only the
flu. Not HIV, not staph, not diptheria, not whooping cough. Only the flu. And then these killer cells can kill other cells that are infected with
the flu. I wont get into how they recognize flu-infected cells, they just do and they kill them. And then some of these killer cells stick around
for decades as memory CD8 T cells - just in case you ever get the flu again, they are there to bounce back and kill it! We also have memory CD4 T
cells and long lived B cells that make antibodies (plasma cells) to fight the flu. But it’s important to understand that the role of cytotoxic T
cells is to kill infected cells, not the virus itself. That’s the antibody’s job. Antibodies are very good at neutralizing viruses and bacteria.
So again, killer T cells kill cells, not the virus. Which is a reason the authors of this study refuse to say this treatment could cure HIV. It can
only cut down on the number of infected cells.