> Not my area of expertise but even if we can address 99% of strains, wouldn't that last 1% just take over and become the new 100% leaving us back where we started?
Yes, this is something to worry about and is exactly the reason why it is so hard to find a cure for AIDS. HIV mutates inside the body into thousands of different configurations and no matter what treatment you throw at it there will generally be at least a couple of strains that will survive and take over.
> Or is the promise here that we can combine this discovery with another that solves that remaining 1%?
That would be hard. There is always a chance that the additional treatment will only treat 99% of that 1% and even a single surviving virus might be enough to restart an infection with resistant strains.
> Or, do the mutations of that last 1% make HIV less virulent or harder to transmit?
One of the other comments here, from someone that read the paper, says that the antibody found in this study binds very specifically to a part of HIV that is crucial for infection so the 1% of strains that resist the antibody (due to mutations in the binding site) are less virulent. The antibody also binds only to parts of HIV that mutate very slowly so it might mean that it would take longer for virulent resistant strains to evolve.
Yes, this is something to worry about and is exactly the reason why it is so hard to find a cure for AIDS. HIV mutates inside the body into thousands of different configurations and no matter what treatment you throw at it there will generally be at least a couple of strains that will survive and take over.
> Or is the promise here that we can combine this discovery with another that solves that remaining 1%?
That would be hard. There is always a chance that the additional treatment will only treat 99% of that 1% and even a single surviving virus might be enough to restart an infection with resistant strains.
> Or, do the mutations of that last 1% make HIV less virulent or harder to transmit?
One of the other comments here, from someone that read the paper, says that the antibody found in this study binds very specifically to a part of HIV that is crucial for infection so the 1% of strains that resist the antibody (due to mutations in the binding site) are less virulent. The antibody also binds only to parts of HIV that mutate very slowly so it might mean that it would take longer for virulent resistant strains to evolve.