Hebrew University of Jerusalem researchers have found how harmful bacteria use a survival strategy that allows it to outsmart the human immune response. This usually results to more intense and persistent infections as well as more effective transmission of the disease person to person.
Phys.org reported that bacteria utilize various strategies to cope with the environments in the organisms they infect. This includes creating adaptive mutations as they evolve as well as initiating specific genes to respond to the changes.
There are times, though, that these defenses are not enough to keep them alive. This is when bacteria turn to alternative strategies.
One particular alternative strategy that has been recently found is the generation of non-genetic variability. This is where bacteria develop sub-populations that are each ready for a different environment or task.
This pre-adaptation would provide invading bacteria a significant advantage during invasion and in defeating the immune system. It is called phenotypic variability, which involves the creation of sub-populations of bacteria with different traits like size or behavior.
The study, which was published in the journal "eLife," was led by Dr. Irine Ronin from the Balaban lab at the Hebrew University of Jerusalem's Racah Institute of Physics. Other researchers involved in the study are Naama Katsowitz, Ilan Rosenshine and Nathalie Q. Balaban.
The scientists investigated whether non-genetic variability contributes to the virulence of a human-specific pathogen, enteropathogenic E. coli (EPEC), which kills several infants worldwide. They wanted to know whether exposing the bacteria to challenging conditions, like in the human body, can trigger it to split into different bacterial sub-populations.
The study revealed that EPEC did spontaneously differentiate into two sub-populations, one of which is virulent when exposed to conditions that copy the host environment. It was found that the hyper-virulent state remains for several generations once triggered. Moreover, the researchers were able to identify the specific regulatory genes that control the switch between the two states of the bacteria.
