perhaps, but it will indeed take gene therapy for this to have any relevance to the vast majority of HIVers

Scientists are being careful about labeling this a "cure" simply because they don't know whether a few years down the road, if there is HIV remaining in his system, it could reactivate and perhaps even switch tropism and he could become ill again (the likelihood of this seems low). However, at this point, it seems like he has been functionally cured. Only time will tell.

Nevertheless, bone marrow transplants are not a viable option for the vast majority of patients with HIV.
- the mortality risk is enormous
- the patients have to be on immunosuppressive drugs for life
- the likelihood of finding a match that contains the CCR5d32 mutation is very low. Only about 1% of people of European ancestry are homozygous for this mutation – it doesn’t seem to be found much (if at all) among other populations. It’s often difficult to find ANY match when a patient needs a bone marrow transplant; once you restrict the list of potential donors to less than 1% of the population, the chance decreases greatly. Since you’re most likely to find a match among people of your own ethnicity, the chance of finding a match with the CCR5d32 mutation will be extremely low for people from populations where the CCR5d32 mutation is rare or nonexistent.

It’s also worth remembering that for many people with HIV, even a successful transplant using matched bone marrow with the mutation will not represent a cure.
For those who don’t already know, in order for HIV to enter a cell, it needs both CD4 and an appropriate chemokine receptor (ever wonder how when you have an infection, your white blood cells know how to get to the right place? Chemokines are the substances that attract them, and they have chemokine receptors for those chemokines that help their cell types home to the right places). HIV can use a variety of chemokine receptors, but the most important ones are CCR5 and CXCR4. Knocking out or blocking CCR5 can confer resistance to HIV infection only for those strains of HIV that use CCR5 to enter cells (these strains are called “CCR5-tropic” or just “R5” – previously, they were referred to as M-tropic, because in test tubes they preferentially infected macrophages, but this is an outdated usage. Still, it’s worth knowing it because you may see it in the literature sometimes). R5 viruses are the ones that transmit most efficiently through sexual contact, and the vast majority (I believe around 80%) of newly infected people have CCR5-tropic viruses. However, in the later stages of infection, only about 50% of people continue to harbor exclusively CCR5-tropic virus. The CCR5d32 mutation (which confers resistance because people homozygous for the mutation do not express CCR5 on the cell surface, therefore denying R5 viruses the receptor they need in order to enter cells) can only protect against R5 viruses, and there have been cases where people homozygous for the mutation nevertheless became infected with HIV (with CXCR4-tropic strains).

Currently, there are drugs available for HIV patients that work by blocking CCR5 (maraviroc, brand name Selzentry). There is also work being done on monoclonal antibodies that perform the same function but could be administered perhaps on a monthly or bi-monthly basis. This could theoretically be used as a prevention strategy for people putting themselves at high risk of infection (i.e. as a sort-of short-term vaccine, but it would not provide perfect protection, since these people would still be subject to infection with non-R5 strains. However, for individuals taking huge risks – i.e. young prostitutes who don’t use protection, young gay men having a lot of unprotected sex with multiple partners – such a preventative strategy could still save a lot of lives). Before a person with HIV begins a CCR5-blocking drug, they have to have a “tropism test” to make sure that their viruses are primarily R5. Many people cannot take the drug because some of the virus in their bodies is not R5 (nearly always because it is CXCR4-tropic, aka X4), and blocking CCR5 just leads through natural selection to the X4 virus becoming predominant.

Blocking CCR5 is safe: People born with the mutation suffer no ill health effects (with one caveat: if infected with West Nile Virus, they appear more likely to develop encephalitis). This is one case where there is enough redundancy built in that the immune system with CCR5 blocked is still fully functional. Patients taking drugs that block CCR5 similarly have shown no major immunological complications. However, it’s unlikely that CXCR4 could be blocked in the same way because patients with genetic defects in CXCR4 signaling do suffer severe effects (e.g. http://www.ncbi.nlm.nih.gov/pubmed/12692554?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=2&log$=relatedarticles&logdbfrom=pubmed
).

Although even gene therapy involving CCR5 wouldn’t represent a cure for a whole lot of people who’ve been living with the virus for a long time, it could finally offer a chance to curb the epidemic.

Gene therapy offers real promise though, since the bone marrow transplant “cure” will never occur in most people with HIV (although rest assured: in the future when people with HIV require bone marrow transplants, they will do everything in their power to try to find a match who is homozygous for the CCR5d32 mutation).

There is actually research going on in this, if anyone is interested:
e.g. http://www.aidsrestherapy.com/content/5/1/16

You’ll find a lot more here if you look!

This bone marrow transplant was surely fascinating, but in order for it truly to offer hope to large numbers of people with HIV, a lot more work needs to be done. We can only hope that in the future, it will be done.

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