A new mechanism that manybacteria use to resist antibiotics has been found by researchers.
The process that some commonly occurring bacteria use to save themselves from the rifamycin class of antibiotics has been discovered using a combination of computation and physical observation.
Rifamycins work by binding to a key part of the bacterium.
The antibiotic can be ejected from the polymerase by the resistantbacteria, which occur in the environment and in some humans. They attack and destroy rifamycin after it is removed.
"What we've discovered is a brand-new trick up the sleeves ofbacteria to evade this class of antibiotics," says researcher Gerry Wright, who leads the GlobalNexus for Pandemics and Biological Threats. It's a one- two punch. It's interesting and it's very clever.
Scientists had previously recognized the mechanisms of antimicrobial resistance, but this discovery shows they are not.
Wright and his colleagues are analyzing tens of thousands of samples to see if otherbacteria use parallel processes and if they reveal vulnerabilities that can be exploited to create new antibiotics.
A paper about their work is online today. Matthew Surette is one of Wright's co- authors.
Wright said the discovery gave him new respect for nature's ability to adapt and renewed his enthusiasm for finding and exposing other methodsbacteria use to ensure their survival
"We've been dealing with this problem for a long time." Every time we think we've figured out all the ways that antibiotics don't work, there's something like this to let us know there are other ways to fight them.
Wright says that the global health concern of AMR should command more attention and resources.
Although the effectiveness of penicillin, rifamycin and other antibiotics is waning, most pharmaceutical companies are not actively developing new antibiotics.
Drug discovery and development costs are high and the financial return on investment in antibiotics is low since they don't generate as much revenue as prescription medications that patients use for years at a time.
Wright says that the threat of public health is too big to ignore.
We need to remind people how difficult these bugs are. We've all been focused on COVID these past two and a half years, but AMR is still an enormous problem and thesebacteria have continued to innovate and broaden their mechanisms of resistance We have to keep trying to understand the enemy.
More information: Gerard D. Wright, HelR is a helicase-like protein that protects RNA polymerase from rifamycin antibiotics., Molecular Cell (2022). DOI: 10.1016/j.molcel.2022.06.019. www.cell.com/molecular-cell/fu … 1097-2765(22)00602-5 Journal information: Molecular Cell
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