To date, scientists are still struggling to understand how some bacteria can penetrate our body's natural defense, our immune system. But, a new study conducted by researchers from the University of Exeter could potentially shed some light into this.
According to new research, severe infections are not necessarily triggered by an increase in the bacteria population.
After getting infected by some pathogens, our resistance to the harmful bacteria eventually grows either with time, vaccines, or antibiotics. Scientists had always assumed that the pathogen responds to this growing immunity by multiplying faster.
But, that’s not true – at least, not entirely.
A new study led by the University of Exeter shows that a pathogen’s virulence – ability to infect or damage a host – can evolve irrespective of its replication rates.
The authors suggested that as we become more resistance, virulence becomes driven by other means. An example of such is the manipulation of the immune system.
In a statement, co-author of the study and researcher at the Centre of Ecology and Conservation on Exeter’s Penryn Campus in Cornwall, Dr. Camille Bonneaud said:
“We typically assume that pathogens respond to host resistance (including to vaccines) by increasing their rate of replication, allowing them to transmit faster to other hosts before their current host clears them.”
Due to human interventions – vaccines and antibiotics – few systems have ever monitored how pathogens evolve in response to a host’s natural resistance. As a result, this field has remained mostly unexplored until now.
Exploring Bacteria Response to the Immune Systems
For the study, the researchers examined how the bacteria, Mycoplasm gallisepticum spreads among house finches.
While some population of the birds has been exposed to the bacteria for over 20 years, others have not. As such, they haven’t developed resistance. Also, since humans have not intervened in any way, the bird provided a perfect way to study host-bacteria evolution.
Findings show that pathogens can evolve to become more virulent without increasing their replication rate.
The researchers noted:
“We hypothesize that the increase in virulence that we observed in this study was driven by an improved ability of the pathogen to manipulate the host immune system in order to generate the symptoms necessary for its transmission.”
According to the authors, this could change how we tackle pathogens.
Instead of trying to kill the pathogens and inadvertently increasing the virulent infections, we could devise a way to slow down its evolution. One way of doing this is to combine treatments that could get rid of the bacteria and also prevent it from manipulating the host immune systems.
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