Tuesday, June 15 at 10:30pm (PDT)Wednesday, June 16 at 06:30am (BST)Wednesday, June 16 02:30pm (KST)
SMB2021 FollowTuesday (Wednesday) during the "CT05" time block.
Faculty of Mathematics, Natural Sciences and Information Technologies, University of Primorska, Slovenia
"The evolution of respiratory disease virulence and diversity"
Theoretical studies of virulence evolution typically assume a positive trade-off between infectivity and harmfulness. This is a valid assumption for diseases where both quantities are determined solely by within-host infection load. However, epidemiological parameters in highly structured host organisms, such as mammals, are largely determined by how the disease agents distribute themselves over body compartments. In respiratory diseases there is even a negative trade-off, with diseases of the lower respiratory tract being both less infective and more harmful. In this talk, we discuss the evolutionary consequences of the interplay between virulence that decreases with an increase in transmission and cross-immunities between pathogen strains. The most salient outcomes of our study are that (i) the upper respiratory tract will support a higher disease diversity, (ii) that emerging respiratory diseases will tend to be more harmful and less infective and (iii) that disease diversity increases with host population density.
Max Planck Institute for Evolutionary Biology
"Evolution of irreversible somatic differentiation"
A key innovation emerging in complex animals is irreversible somatic differentiation: daughters of a vegetative cell perform a vegetative function as well, thus, forming a somatic lineage that can no longer be directly involved in reproduction. Primitive species use a different strategy: vegetative and reproductive tasks are separated in time rather than in space. Starting from such a strategy, how is it possible to evolve life forms which use some of their cells exclusively for vegetative functions? Here, we developed an evolutionary model of development of a simple multicellular organism and found that three components are necessary for the evolution of irreversible somatic differentiation: (i) costly cell differentiation, (ii) vegetative cells that significantly improve the organism's performance even if present in small numbers, and (iii) large enough organism size. Our findings demonstrate how an egalitarian development typical for loose cell colonies can evolve into germ-soma differentiation dominating metazoans.
Tel Aviv University
"Non-Vertical Cultural Transmission , Assortment , and the Evolution of Cooperation"
We present a model for the evolution of cooperation under vertical, horizontal, and oblique cultural transmission. We find that the evolution of cooperation is facilitated by its horizontal transmission and by an association between social interactions and horizontal transmission. The effect of oblique transmission depends on the horizontal transmission bias. Stable polymorphism of cooperation and defection can occur, and when it does, reduced association between social interactions and horizontal transmission evolves, which leads to a decreased frequency of cooperation and lower population mean fitness. We compare our results to outcomes of stochastic simulations of structured populations. Parallels are drawn with Hamilton's rule incorporating assortment and relatedness.
Max Planck Institute for Evolutionary Biology, Plön, Germany
"Within-host evolution of antibiotic resistance under sequential therapy"
The rapid evolution of antibiotic resistance and the resulting loss in treatment options call for the development of sustainable treatment strategies. Supported by laboratory experiments, alternating antibiotics during treatment has been proposed as a promising approach. Evolutionary trade-offs, especially collateral sensitivity, could potentially further improve the outcome.A limitation of in-vitro evolution experiments is that they do not account for the complex environment of the patient's body. Drugs persist in the body for some time at continuously decreasing concentrations, leading to a temporal overlap of the drugs in a cycling schedule. It is a priori not clear how drug-drug-interactions during these periods of drug overlap influence the outcome of sequential therapy. To close this gap, we set up a pharmacokinetic-pharmacodynamic model that incorporates drug-drug-interactions. We aim to reveal the treatment settings that optimize the outcome of sequential therapy, given the risk of resistance evolution. Our results suggest that drug-drug-interactions strongly influence the optimal protocol. For synergistic drugs pairs, rapid switching of drugs minimizes the time to eradication of the pathogen population. For antagonistic drugs, the decision is not as straightforward, and switching the drugs less often is sometimes preferable. Collateral sensitivity only improves the efficiency if cycling is slow.