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mutations that can impact virulence? examples of pathogens/virulence genes where each type of mutation process is...

mutations that can impact virulence?

examples of pathogens/virulence genes where each type of mutation process is important for evolution?

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A mutation in the gyrA gene of UPEC causes a decrease in the virulence of the bacteria due to the effect of DNA supercoiling on the expression of several virulence factors and proteins, thereby decreasing the capacity to cause cystitis and pyelonephritis. The evolution of pathogens presents a paradox. Pathogenic species are often absolutely dependent on their host species for their propagation through evolutionary time, yet the pathogenic lifestyle requires that the host be damaged during this dependence. It is clear that pathogenic strategies are successful in evolutionary terms because a diverse array of pathogens exists in nature. Pathogens also evolve using a broad range of molecular mechanisms to acquire and modulate existing virulence traits in order to achieve this success. Detailing the benefit of enhanced selection derived through virulence and understanding the mechanisms through which virulence evolves are important to understanding the natural world and both have implications for human health.

The evolution of parasite virulence can be influenced by intra-host mutation of the parasite and competition among different parasite mutants in the same host. During the course of an infection, parasite variants may be generated that have some competitive advantage over the strains that initiated the infection. This intra-host competition may select for a short-term advantage. It can lead to variants without any transmission potential or variants with extremely high virulence. The major conclusions are: (i) intra-host competition generates a virulence polymorphism in the parasite population; (ii) intra-host competition can shift the mean virulence beyond what would maximize the reproductive rate of the parasite in the host population; and (iii) the parasite population can evolve to intermediate levels of virulence even if there is no trade-off between transmission rate and virulence. This applies to highly mutating parasites with long infection periods, such as, for example, the human immunodeficiency virus (HIV).


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