TAU researchers develop method to fight bacteria resistant to antibiotics

The researchers published their findings in the scientific journal PNAS - Proceeding of the National Academy of Sciences.

Elongation of bacteria due to inhibition of division is caused by the bacteriophage protein. (photo credit: DR. TRIDIB MAHATA)
Elongation of bacteria due to inhibition of division is caused by the bacteriophage protein.
(photo credit: DR. TRIDIB MAHATA)
Researchers at Tel Aviv University (TAU) have developed a process by which "good" viruses can attack the systems of "bad" bacteria, according to a university statement.
The method discovered could in turn destroy and affect reproduction capabilities of the bacteria by blocking the replication mechanism of the bacteria's DNA without damaging its own - distinguishing good viruses from the bad bacteria, which could be put forth towards a further understanding of bacterial mechanisms for evading bacteriophages and using bacteriophages to combat bacteria.
Antibiotic resistance of bacteria is a challenge that many scientists face today. The TAU researchers purport that a potential solution for this problem lies within further investigation of the discovered process, most importantly understanding the "bacteriophage mechanisms for taking over bacteria as a basis for the development of new tools to combat bacterial pathogens," the university said.
Keeping this notion in mind the researchers unveiled the said mechanism and found that the bacteriophage protein works off of a DNA-repair protein in the bacteria to "cut the bacteria's DNA as it is being repaired," TAU added.
"The bacteriophage takes advantage of the bacterial DNA's need for repair, while the bacteriophage itself has no need for this specific kind of repair," said Prof. Udi Qimron, one of the lead authors of the study. "In this way the bacteriophage destroys the bacteria without suffering any damage to itself."
"The ability to distinguish between oneself and others is of enormous importance in nature and in various biological applications," Qimron added. "Thus, for example, all antibiotic mechanisms identify and neutralize bacteria only, with minimal effect on human cells. Another example is our immune system, which is geared toward maximum damage to foreign factors, with minimal self-injury."
The researchers developed a process for searching for types of bacterial variants not impacted by this mechanism, being those who have developed immunity to it, which led them to the discovery of the specific bacterial mechanism affected by bacteriophage takeover.
"We found that the 'immune' bacterial variants simply stopped repairing their DNA in ways that are vulnerable to the bacteriophage attack, thereby evading the bacteriophage's destructive mechanism. Shedding more light on the ways in which bacteriophages attack bacteria, our findings may serve as a tool in the endless battle against antibiotic-resistant bacteria," concluded Qimron.
The researchers published their findings in the scientific journal PNAS - Proceeding of the National Academy of Sciences.