Re: Immune to HIV?
I didn't see the interview. Usually when the popular media is talking about natural immunity to HIV, they are talking about people who are homozygous for the CCR5-delta32 mutation. That means that they got a "defective" copy of the CCR5 gene from both their mother and their father. This CCR5 mutation is not uncommon in people of European ancestry - about 1 in 5 have one copy of the mutated gene, but only 1% have two defective copies (the defective gene probably is common in certain populations because it provided a survival advantage - i.e. resistance - to other infectious diseases that killed a lot of Europeans hundreds of years ago. Smallpox and bubonic plague have received a lot of attentions as likely candidates).
So, to infect a cell (a T-cell say), HIV needs to get inside it. To do so, it attaches to surface receptors. I won't go too deep into the details, but basically, to get inside a T-cell, HIV must attach to both a CD4 receptor and a chemokine receptor. Most HIV viruses use the CCR5 receptor - these viruses are called "CCR5-tropic". If a person has 2 defective copies of the CCR5 gene, they will not express CCR5 on the cell surface (it is like a door without a keyhole. HIV has the key to get inside but the keyhole has been removed, so it cannot stick the key in, and unlock the door to get inside).
So, does the fact that some people are genetically resistant to HIV infection help us find a cure? Yes and No.
First, they are not quite "immune". They are resistant, and they are not actually fully resistant. They can still be infected by strains of HIV that use different chemokine receptors (and in fact, some of them have, and some of them have died from it). CCR5-tropic viruses are the most commonly transmitted viruses, but those who are homozygous for the CCR5-delta32 mutation should not think that they cannot get HIV. They're less likely to catch it than other people, but they still are susceptible.
But that's not really here nor there. Does it help us find a cure?
If by "cure", you mean a way to completely and permanently eradicate HIV in people who are already infected, this seems unlikely (because no matter what you do with CCR5, this is unlikely to get rid of the cells that are already infected). But we already are taking a cue from those who naturally resistant to HIV, and they have very much helped us in coming up with at least one effective treatment: blocking CCR5. Since many people in the population do not express CCR5 receptors (large in absolute numbers, although small as a percentage), and they are perfectly healthy as far as anyone can tell (with one exception: when they're infected with West Nile Virus, they get sicker than other people), blocking CCR5 seemed safe, and experience thus far has borne this out: it appears to be incredibly non-toxic and has side-effects equivalent to placebo. It is not, however, a cure, and like with everything else, HIV can eventually mutate around it, and will do so quickly if it is used alone.
A longer-term possibility (which is years away, but technology proceeds at such a rapid pace, that you never know!) would be genetic therapies or vaccines that could make those who have not yet been infected resistant to CCR5-tropic strains. They've already made monoclonal antibodies that block CCR5 (these may be available in the future instead of medications for those who are infected, to take on a monthly or bi-monthly basis), but nobody wants to take a shot every month as prevention, even if it is side-effect free. The problem with stimulating a natural immune response to CCR5 (i.e. stimulating autoimmunity with a vaccine) is that this would cause death of those cells that the receptors were on, rather than just blocking viral entry (because in a laboratory, you can engineer "defective" antibodies. Antibodies themselves do not directly kill germs or cells. They act in many ways to help your body get rid of germs, and one of the things they do is attract other cells that DO kill germs. When a germ is covered in antibodies, other cells will eat the germ or attack the germ much more readily. Antibodies are like chocolate sauce. They make the germ more tasty. In the laboratory, you can make an antibody that is specific to the CCR5 receptor, but that does NOT taste like chocolate sauce [for those who prefer not to speak in analogies, it generally lacks an Fc region], so other cells will not come and gulp up that T-cell. Stimulating a real immune response with a vaccine would be much more problematic (caution is obviously warranted in triggering autoimmunity, although one could imagine technological possibilities... This is outside of my realm, however.)
I could write a whole lot more on this, but I am on my way out for the evening and I probably should've left 5 minutes ago.
Hope you're doing well!