ericans.
What about some gene therapy then, if one mutation provides protection? The article merely notes that Professor Duncan, one of the authors, “is not hopeful that the genetic mutation, can be reproduced artificially to create protection”.
HIV Immunity
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groups to be added to the promoter DNA, switching the gene off permanently.
No one had ever shown that this happens in mammalian cells. “If it wasn’t for a couple of tricks, we also might not have found it,” says Morris. Because of his interest in HIV, Morris used a related virus called feline immunodeficiency virus (FIV) to add an extra gene to human cells. Then he tried targeting its promoter sequence with siRNAs. The team found that the promoter sequence did become methylated, turning off the gene permanently.
However, if an existing gene was targeted, rather than one delivered by FIV, the promoter sequence did not become methylated. Additional studies suggest that FIV plays a crucial role, opening up the cell nucleus so the siRNAs can reach the promoter sequence (Science , DOI: 10.1126/science.1101372).
“It’s a very exciting result to find this same mechanism shared by plants, yeast and now humans. The therapeutic implications are huge,” says Robert Martienssen, an RNAi researcher at Cold Spring Harbor Laboratory, New York.
Methylation plays a key role in reproduction and development; it may be one reason why cloning is so difficult, for instance. No one understands how the process is controlled, but Martienssen suggests that our cells might control methylation by producing their own siRNA-like molecules.
Some researchers are sceptical. If this type of silencing does not work without FIV, they point out, it probably does not normally take place in cells. And many labs have failed to see similar results despite massive efforts.
These issues should be resolved quickly. Several attempts to replicate these experiments are already under way. “There are a lot of people working on this,” says Morris.
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