I came here to say the same thing, it is a very well written story in my opinion, which manages to be accessible, while at the same time retaining accuracy. Well done Jacquelyne Froeber and the editors who worked on the copy.
As for whether this is a big deal: Yes - in terms of science, although not necessarily a big clinical deal. Other strains may use different receptors, but this is the most common. There is also the mystery question embedded in the story: Why didn't the other strain he was infected woiith rebound
I just read the New England Journal report. He wasn't infected with another strain. Strictly, everyone with HIV is infected with a distribution of strains because it random mutations happen. The virus can bind either the CCR5 receptor or the CXCR4 receptor. As pressure on the CCR5 pathway increases, survival of CXCR4-tropic variants becomes more pronounced. Essentially, CCR5 is the easier and more common target of the virus, so the wildtype tends to equilibrate toward a cluster of strains that favor CCR5. It's simply more energetically efficient for the virus. It's a thermodynamic equilibrium. In fact, the report explains this. As HAART therapy is used to suppress the virus, the surviving viral genes get better and better at binding CXCR4 and it is a well observed part of the natural course of the disease that CXCR4-tropism develops late in the course of the disease. The patient lives longer with HAART therapy, but dies of a slightly different disease than they were infected with. It's very much the same sort of evolutionary thing that happens with other, less exotic forms of bacterial antibiotic resistance.
The big deal, intellectually, for me, is the clear-cut experiment that shows just how dependent on CCR5 the virus really is. Now in my fourth year of medical school, the professors have always been hedging their statements: well CCR5 is a known tropic factor, but we really don't know how big a deal it is, and then there's CXCR4, and maybe there's other factors, so we really don't know.
Compare that to "took him off HAART and the virus came back like a ton of bricks. Reapplied HAART and the virus regressed. Coincidentally, we took the CCR5 receptor site out of his system, then took him off HAART again, and we get an entirely different response: no virus, and any evidence that there ever was a virus is slowly fading from his system".
Hopefully there will be other advances in how to kill the HIV, but this very much a lightswitch sort of event for medicine.
As for whether this is a big deal: Yes - in terms of science, although not necessarily a big clinical deal. Other strains may use different receptors, but this is the most common. There is also the mystery question embedded in the story: Why didn't the other strain he was infected woiith rebound