This science behind this is actually seriously interesting.
A small % of European populations are immune to HIV - it's thought that the same mutation provided some protection against the plague. If a person with HIV receives a bone marrow transplant from someone who is immune, their new blood cells are immune. This was first discovered in a man known as the "Berlin patient", who suffered from both leukemia and HIV. The bone marrow transplant was administered to treat his cancer, and it wound up curing his HIV.
The problem is that finding a bone marrow donor is tough enough as it is, let alone someone who happens to have the correct mutation. As well as that, people with HIV tend to have a normal life expectancy with correct medication, where as bone marrow transplants have a 15-20% mortality rate. With those sorts of numbers, it's very difficult to get ethical approval for a trial.
More info: http://www.guardian.co.uk/society/2013/jul/03/hiv-bone-marrow-transplant
Cornelo Prisan you are correct, although as you pointed out, the mechanism of that cure probably was different, both because the drugs were started almost immediately post infection (which happens during birth) and that the infant immune system is quite different then adults at least during the first year of life.
ReplyDeleteThe challenge is to come up with methods to both target latently-infected T cell reservoirs and also block any new infections happening in the same person. While "Berlin Patient" and above transplant patients are great proof-of-principles a cure can be achieved, they are not practical (with lot of side effects) on general HIV-infected population.
Thus, we are actually also developing a different approach to eliminate the cells that express CCR5, which is the receptor for HIV and is mutated in about 1% of northern European population (we recently published a paper, where we speculated why that mutation arose). Many other labs are also working towards this goal with different approaches. We will probably find general HIV cure before a vaccine.
What about the CD4 and CXCR4 receptors?
ReplyDeleteAmazing!
ReplyDeleteJames Williams Expression of CD4 alone on the cell surface is not sufficient for HIV-1 to enter into the cells, so it requires one of the co-receptors CCR5 or CXCR4. The reason, why CCR5 is much more important is because it is required for transmission of the virus (thus 1% of Northern Europeans who have mutation on CCR5 are completely resistant to transmission) and most HIV strains, until late in infection, utilize CCR5. Although in a subset of untreated HIV+ subjects eventually CXCR4-using viruses or what we call dual-tropic (can use both receptors) ones evolve, it is not clear if targeting CCR5 alone would be sufficient to cure those. At this point, we celebrate even couple of these people who had appear to have been completely cured of infection, as this has been such a tough nut to crack ...
ReplyDeleteDerya Unutmaz Thanks for the information! I currently work with other viral systems, but I have tried to assist others with structural studies on HIV Env glycoprotein. I am only recently becoming familiar with the attachment/fusion process.
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