Antibiotic Resistance Develops After Deadly Bacteria Mimics Human Proteins

by Kathy Jones on  June 3, 2011 at 8:15 PM Research News   - G J E 4
Deadly bacteria may mimic human proteins to evolve antibiotic resistance, a new study has revealed.
 Antibiotic Resistance Develops After Deadly Bacteria Mimics Human Proteins
Antibiotic Resistance Develops After Deadly Bacteria Mimics Human Proteins

"This mimicry allows the bacteria to evade its host's defence responses, side-stepping our immune system," said Dr. Mia Champion, an Assistant Professor in TGen's Pathogen Genomics Division, and the study's author.

Using genomic sequencing, the spelling out of billions of genetic instructions stored in DNA, the study had identified several methyltransferase protein families that are very similar to human bacterial pathogens.

Researchers found methyltransferase in the pathogen Francisella tularensis subspecies tularensis and just one cell could be lethal.

Similar methyltransferase proteins are found in other highly infectious bacteria, including the pathogen Mycobacterium tuberculosis that causes Tuberculosis.

"Altogether, evidence suggests a role of the Francisella tularensis protein in a mechanism of molecular mimicry. Upon infection, bacterial pathogens dump more than 200 proteins into human macrophage cells called effector proteins," Dr. Champion said.

'"Because these proteins are so similar to the human proteins, it mimics them and enables them to interfere with the body's immunity response, thereby protecting the pathogen.

"These findings not only provide insights into the evolution of virulence in Francisella, but have broader implications regarding the molecular mechanisms that mediate host-pathogen relationships," she added.

Dr. Champion also said that identifying small differences between the pathogen and human proteins through next generation genome-wide datasets could help develop molecular targets in the development of new drug treatments.

The study done by the 'Translational Genomics Research Institute' (TGen) , was published in the journal 'Public Library of Science' (PLoS) One.

Source: ANI

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