We are searching data for your request:
Upon completion, a link will appear to access the found materials.
Scientists are fighting what sometimes feels like an uphill battle against antibiotic resistance. They seem to have a new weapon in their arsenal, though: naturally occurring viruses called bacteriophages that are capable of infecting and killing bacteria.
These viruses can be modified to target certain types of bacteria specifically. What's more, bacteriophages kill bacteria through different mechanisms than typical antibiotics.
RELATED: GENETICALLY ENGINEERED VIRUS JUST SAVED THE LIFE OF PATIENT WITH DRUG-RESISTANT INFECTION
In a new study, biological engineers from MIT showed that they could quickly program bacteriophages to target and kill different strains of E. coli. They did so by making mutations in a viral protein that binds to host cells.
An added benefit the researchers found is that the engineered bacteriophages are also less likely to provoke resistance in bacteria.
“As we’re seeing in the news more and more now, bacterial resistance is continuing to evolve and is increasingly problematic for public health,” Timothy Lu, an MIT associate professor of electrical engineering and computer science and biological engineering, said in a press release.
“Phages represent a very different way of killing bacteria than antibiotics, which is complementary to antibiotics, rather than trying to replace them.”
Engineering life-saving bacteria
The researchers created several different engineered bacteriophages that were able to kill E. coli.
Most importantly, one of the newly engineered bacteriophages was able to destroy two E. coli strains, that are resistant to the naturally occurring unmodified bacteriophage.
The research paper was published in Cell. In the future, the researchers hope to use this targeted method to take on other strains of bacteria, such as those that live in the human gut.
Work in bacteriophages is extremely promising and has previously saved the life of a patient who was showing resistance to all other treatments.
“This is just the beginning, as there are many other viral scaffolds and bacteria to target,” says Kevin Yehl, one of the study's lead authors.