scholarly journals Adaptive Evolution of Virulence-Related Traits in a Susceptible-Infected Model with Treatment

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Xinzhu Meng ◽  
Yang Yang ◽  
Shengnan Zhao

Evolution problem is now a hot topic in the mathematical biology field. This paper investigates the adaptive evolution of pathogen virulence in a susceptible-infected (SI) model under drug treatment. We explore the evolution of a continuous trait, virulence of a pathogen, and consider virulence-dependent cure rate (recovery rate) that dramatically affects the outcome of evolution. With the methods of critical function analysis and adaptive dynamics, we identify the evolutionary conditions for continuously stable strategies, evolutionary repellers, and evolutionary branching points. First, the results show that a high-intensity strength drug treatment can result in evolutionary branching and the evolution of pathogen strains will tend towards a higher virulence with the increase of the strength of the treatment. Second, we use the critical function analysis to investigate the evolution of virulence-related traits and show that evolutionary outcomes strongly depend on the shape of the trade-off between virulence and transmission. Third, after evolutionary branching, the two infective species will evolve to an evolutionarily stable dimorphism at which they can continue to coexist, and no further branching is possible, which is independent of the cure rate function.

Author(s):  
Bing Liu ◽  
Le Song ◽  
Xin Wang ◽  
Baolin Kang

In this paper, we develop a single species evolutionary model with a continuous phenotypic trait in a pulsed pollution discharge environment and discuss the effects of pollution on the individual size of the species. The invasion fitness function of a monomorphic species is given, which involves the long-term average exponential growth rate of the species. Then the critical function analysis method is used to obtain the evolutionary dynamics of the system, which is related to interspecific competition intensity between mutant species and resident species and the curvature of the trade-off between individual size and the intrinsic growth rate. We conclude that the pollution affects the evolutionary traits and evolutionary dynamics. The worsening of the pollution can lead to rapid stable evolution toward a smaller individual size, while the opposite is more likely to generate evolutionary branching and promote species diversity. The adaptive dynamics of coevolution of dimorphic species is further analyzed when evolutionary branching occurs.


2019 ◽  
Author(s):  
Hiroshi C. Ito

AbstractSome evolutionary traits are described by scalars and vectors, while others are described by continuous functions on spaces (e.g., shapes of organisms, resource allocation strategies between growth and reproduction along time, and effort allocation strategies for continuous resource distributions along resource property axes). The latter are called function-valued traits. This study develops conditions for candidate evolutionary branching points, referred to as CBP conditions, for function-valued traits under simple equality constraints, in the framework of adaptive dynamics theory (i.e., asexual reproduction and rare mutation are assumed). CBP conditions are composed of conditions for evolutionary singularity, strong convergence stability, and evolutionary instability. The CBP conditions for function-valued traits are derived by transforming the CBP conditions for vector traits into those for infinite-dimensional vector traits.


Blood ◽  
2009 ◽  
Vol 114 (23) ◽  
pp. 4804-4812 ◽  
Author(s):  
Erin A. Kimbrel ◽  
Madeleine E. Lemieux ◽  
Xiaobo Xia ◽  
Tina N. Davis ◽  
Vivienne I. Rebel ◽  
...  

Abstract Cyclic adenosine monophosphate response element binding (CREB)–binding protein (CBP) and p300 are multidomain transcriptional coactivators that help assemble large regulatory complexes at sites of active transcription. Nullizygosity of CBP or p300 results in pervasive defects in hematopoiesis. To systematically assess the structural domains of p300 required for normal hematopoiesis, we used recombinase-mediated cassette exchange to create an allelic series of coisogenic embryonic stem cells, each expressing a different mutant of p300 from the endogenous locus. We found that deletion of either the KIX or CH1 domain caused profound and pervasive defects in hematopoiesis, whereas the loss of most other domains had only lineage-restricted effects. When expressed from the p300 locus, an extra copy of CBP largely compensated for a lack of p300. Surprisingly, mutation of the p300 histone acetyltransferase (HAT) domain had minimal effects on hematopoiesis, and actually increased progenitor and stem cell numbers and proliferative potential. Our results suggest that, in distinct contrast to other organ systems, HAT activity does not provide a critical function for hematopoietic development and emphasizes the importance of enzyme-independent functions of p300.


2010 ◽  
Vol 266 (4) ◽  
pp. 529-535 ◽  
Author(s):  
Michael Doebeli ◽  
Iaroslav Ispolatov

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