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Evolutionary Biology of Parasitism
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2023
Eric S. Loker, Bruce V. Hofkin
It has been argued that virulence proceeds in three phases, with the first being a new contact between a particular parasite and host. Although many such contacts fail, some proceed to phase 2 during which virulence, not being settled at an optimum level, is likely to evolve rapidly. Phase 2 can be characterized by spectacular emergence of devastating new pathogens, witness the emergence from zoonotic origins of Ebola virus or SARS-CoV-2 for example. Resultant epidemics are accompanied by selection that modifies the parasite’s life history, transmission and virulence, and may lead to endemic disease status, enabling prolonged relatively benign coexistence with its host. Here we must give the traditional idea that parasites “evolve to be less virulent” some credit, for this outcome may occur. However, because it was realized that some parasites long associated with their hosts such as tuberculosis in humans remain virulent, the conventional wisdom began to give way to the idea that natural selection should favor virulent forms if they are more immediately successful. According to the phase model, it is only in phase 3, the evolution of “optimal virulence,” when equilibrium conditions have been established, that trade-offs begin to apply.
Enteropathogenic Escherichia coli regulates host-cell mitochondrial morphology
Published in Gut Microbes, 2022
Jennifer Lising Roxas, Shylaja Ramamurthy, Katie Cocchi, Ilga Rutins, Anusha Harishankar, Al Agellon, John Scott Wilbur, Gresa Sylejmani, Gayatri Vedantam, V.K. Viswanathan
Collectively, our data and the published literature show that EPEC, an extracellular pathogen, orchestrates intestinal epithelial mitochondrial alterations, and this could underlie the critical requirement of effector proteins like EspZ and EspH for optimal virulence of A/E pathogens.