g cells and tissues thus allowing the bacteria to break out and spread through the body.
Applying the pressure of natural selection, the human immune system normally would clear a localized infection. But in the case of the M1T1 strep clone, natural selection instead favors the emergence of the invasive mutants.
The researchers found that a specific genetic mutation in the M1T1 strep clone controls the shift to this invasive form a property which they traced to an event that occurred about 30 years ago when a virus known as a bacteriophage infected the strep bacteria and introduced a new gene. The new gene allowed the bacteria to resist clearance by the human immune system.
Our study provides a model of how natural selection, exerted by the human immune system, can generate hypervirulent bacterial variants with an increased risk of producing invasive infections, said lead author Mark Walker, Ph.D. a Professor of Biological Sciences at the University of Wollongong.
In the case of the invasive strep clone, a bacteriophage provided the bacterium a genetic advantage that turned a relatively benign pathogen into a potential deadly disease agent.
A gene present on the bacteriophage acquired by the M1T1 strep encodes an enzyme that allows the bacteria to escape being trapped and killed by neutrophils white blood cells that play a front line role in humans immune defense by pathogenic microbes.
The same genetic mutation that allows the strep bacteria to acquire plasminogen and activate it throughout the body also increases production of the bacteriophage-encoded enzyme that blocks neutrophil killing.
When neutrophils of the immune system are summoned to clear a simple strep infection, they apply a natural selective pressure favoring the genetic mutation.
The mutation allows the bacteria not only to survive neutrophil killing, but to spread and destroy tissues, Page: 1 2 3 Related medicine news :1
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