UCLA research uncovers 'smart antibiotics'

A new generation of 'smart antibiotics', which uses a virus that
adapts to recognize and attack bacteria, could become the latest
approach to tackling the growing public health problem of
antibiotic-resistant pathogens such as methicillin-resistant
Stapholococcus aureus (MRSA) and vancomycin-resistant Enterococci
(VRE).

This latest research opens up numerous possibilities for developing drugs and vaccines that can control resistant bacteria. The problem with current antibiotics is while bacteria can mutate and become resistant to a particular antibiotic, the antibiotic is static and cannot modify its mechanism.

UCLA microbiologists discovered the new class of genetic elements, similar to retroviruses that operate in bacteria allowing them to diversify its proteins to bind to a large variety of receptors. The team discovered this fundamental mechanism in bacteriophages, the viruses that infect bacteria.

They found that the bacteriophages contain genes that allow them to quickly change their proteins to bind to different cell receptors. The researchers, who encountered this genetic property while working on an unrelated project, believe this discovery could lead to the use of genetically engineered phages.

Jeffrey Miller, professor of microbiology at the University of California and lead researcher said: "We now think we can engineer bacteriophages to function as 'dynamic' anti-microbial agents."

"This could provide us with a renewable resource of smart antibiotics for treating bacterial diseases."

The introduction of bacteriophages may also lead to a unique approach against biodefense-related pathogens.

Miller's team had found the genome of the phage that infected Bordetella bronchiseptica, contained a series of genes that changed the part of the virus that binds to the bacterial cell. These genes allow the phage to rapidly evolve new variants that can recognize and attack bacteria that may have become resistant to the previous phage.

Through bioinformatics and analysis of DNA sequences, Miller's team has found evidence for many other cases where either bacteriophage or bacteria use the same strategy for targeting mutations and speeding up evolution.

Miller said that they were continuing to study the genetic mechanism to learn more about its biochemical properties and to determine whether higher forms of life have similar classes of genes.

"In time will be able to use the knowledge gleaned from this discovery to generate proteins in the laboratory that will bind to almost any molecule of interest."

"We think we can make proteins that bind to peptides, and make peptides that bind to larger proteins,"​ he said.

Nearly 2 million people in the United States will acquire bacterial infections while in the hospital, and about 90,000 of them will die, according to estimates from the Centres for Disease Control and Prevention (CDC).

More than 70 per cent of the bacteria that cause these infections will be resistant to at least one of the drugs commonly used to fight them. Even more alarming, resistant bacteria such as methicillin-resistant Staphylococcus aureus (MRSA) are beginning to strike healthy people outside of hospitals.

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