Fascinating bit of hi-tech medicine. Stymied in efforts to create new drugs for drug-resistant tuberculosis, biologists have taken a very close look at the genetic mechanism for the resistance to one particular drug, Ethionamide. Ethionamide only becomes dangerous when bacteria metabolize it into a different compound, and the drug resistance comes from turning off the gene that directs the cell to metabolize Ethionamide. But there is actually another gene that can be made to do the same thing. That gene is not usually very active, but when prodded using a custom molecule called SMARt-420 it become active, starts metabolizing Ethionamide, and the cell dies.
This suggests that the future of antibiotic medicine will not be developing new poisons in a race against bacterial resistance, but developing ways to mess with bacterial genomes that interfere with their evolution of resistance.
How well can we control evolution?
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2 comments:
Why bother dosing bacteria with a custom molecule that causes them to become vulnerable to an entirely separate antibacterial compound, when you could just use a different custom molecule to cause a genetic error that kills them outright without the need for any separate compound at all?
Or put more simply, why use a genetic tampering to make them vulnerable to a poison, when you could instead just use genetic tampering by itself AS a poison?
I suspect that's coming.
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