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Published online 2 March 2009 | Nature | doi:10.1038/news.2009.131
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Engineered viruses fight bacteria
Viruses that target bacteria could help give antibiotics a boost.
Biologists have engineered viruses to weaken the bacteria they infect, leaving the bugs more vulnerable to antibiotics. With more bacteria becoming resistant to the most commonly used antibiotics, the viral approach could extend the useful lifetime of these drugs.
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"But bacteria under this kind of direct attack quickly evolve to become resistant to the phage." That is a true statement but have you ever checked the numbers? E.coli can become resistant to rifampicin or fluroquinolones much more easily than it bacomes resistant to many phages. And just like rifampicin (which is one of the best antibiotics) we can do cocktails of different phages. "Instead of using lethal viruses, they engineered their viruses to just weaken the bacteria, making them more susceptible to antibiotics. ... When the modified M13 phage infects a bacterium, in this case Escherichia coli, it produces lexA3, which renders the bacterium more vulnerable to DNA-damaging drugs." This approach is not understandable. Why not use directly genes that encode for very powerfull toxins (there are hundreds of them...) like ccdB and directly kill the bacterium? " The researchers found that the phage increased the ability of the antibiotic ofloxacin to kill E. coli grown in culture, even when the bacteria were resistant to the antibiotic on its own. The findings suggest that this type of phage therapy could rejuvenate antibiotics that have been deemed no longer effective. " So the story is to use expensive antibiotics although the phage could kill the bacteria on its own. "Despite its long history, there are lingering concerns about phage therapy. The treatment could trigger an unwanted immune response, for example, or some phages may not survive the trip through the human body to their target cells." That is 100% true, but for every bacterium species you can find thousands of different phages. Some of them though are only specific to some strains. So it is far easier to find phages that have all the desired properties than to find antibiotics with the desired properties. All in all the paper does not propose the best approach. It proposes an approach that the pharmaceutical companies will like because they can patent the new cocktail (old antibiotic + phages). It simply makes no sense to sensitize bacteria to antibiotics. It makes much more sense to directly kill them.
After reading the paper I noticed this "Eighty percent of mice that received philexA3 with ofloxacin survived, compared with 50% mice that received phiunmod plus ofloxacin and 20% of mice that received ofloxacin alone". Now this is something. Unmodified virus helps a lot!!! Meaning the virus has its own genes that cripple the bacterium. LexA3 is just a little help