The ability to reawaken retrocyclin genes from their 7 million years of slumber using aminoglycosides could provide a novel way to secure enhanced resistance to HIV-1 infection.
After 7 million years of no selective pressure, these genes have certainly accumulated mutations. I would put my money on the "resurrected" protein being completely useless.
The genome is full of random crap left over from the evolutionary process (including some things thought to have been captured from viruses). Who knows what kinds of selective pressure this section of the genome has been exposed to? It has obviously accumulated some amount of mutations, hence the premature stop codon.
It is important to note that the retrocyclin is correctly produced in old world monkeys, and the mRNA is created in humans (as a pseudo gene). So, the lack of selective pressure is a pretty recent event (evolutionarily).
So, this _is_ science, no 'technically' about it. PLoS is a top tier journal, and this looks very promising. So while this may not be a 'cure' for those with HIV, it could very well help people avoid an initial infection.
Who knows what kinds of selective pressure this section of the genome has been exposed to?
Probably none. You would be hard pressed to conjure up a reason to explain why a sequence that codes for a non-functional protein would be functionally conserved for 7 million years. (You could win a Nobel prize for such a revolutionary contribution.)
I work in drug design. Let me assure you that even a single mutation can render the structure of a protein completely inert.
There is also no reason why it wouldn't be conserved... perhaps it's in a highly conversed region? Without looking up exactly where it is in the genome, I wouldn't speculate. I'd be more interested in knowing how the sequences compared to chimp or orangutan.
I'm fully aware that a single mutation can render a protein inert. However, a different mutation might not have any effect. In this case, the mRNA is expressed as a pseudo-gene, so that's a good sign. The mutation is a nonsense truncation. With that problem 'fixed' and with a correctly translated protein, this protein might still work.
The ability to reawaken retrocyclin genes from their 7 million years of slumber using aminoglycosides could provide a novel way to secure enhanced resistance to HIV-1 infection.
After 7 million years of no selective pressure, these genes have certainly accumulated mutations. I would put my money on the "resurrected" protein being completely useless.