arXiv subjects

Yaroslav Ispolatov

Publications and source records attributed to Yaroslav Ispolatov.

5 recordsLinked to original sources

arXiv2026

Evolution of cooperation in spatially structured group-selection models of the continuous Prisoner's Dilemma

We consider continuous Prisoner's Dilemma games played in a spatial setting by group-structured populations. The evolutionary dynamics is driven by within-group individual-level birth and death events, and by group-level fission and extinction events. Within groups, individuals play well-mixed games, while groups play games on a 1-dimensional spatial grid against their nearest neighbours. Payoffs from individual-level games affect birth rates of individuals, and payoffs from group-level games affect group extinction and fission probabilities. It is well known that the within-group evolution by itself always results in a complete loss of cooperation, and that in the group-level games, defection is also favoured if these games are played in well-mixed populations of groups. Here we show that despite this double disadvantage, cooperation can be maintained due to spatially structured group-level dynamics. Mirroring results from one-level selection models, the spatial nature of games between groups and the resulting fissioning and extinction events is essential for the evolution of cooperation in these models, but needs to manifest itself in specific ways in order to be effective: we find that higher levels of cooperation evolve when the selection generated by games between groups acts locally rather than globally.

q-bio.PE↗

arXiv2025

Epidemiological dynamics with clinically-derived infectiousness and incubation time courses

To better predict the dynamics of epidemics such as COVID-19, it is important not only to investigate the network of local and long-range contagious contacts but also to understand the temporal dynamics of infectiousness and detectable symptoms. Here, we present a model of infection spread in a well-mixed group of individuals, which usually corresponds to a node in large-scale epidemiological networks. The model uses delay equations that take into account the duration of infection and are based on experimentally derived time courses of viral load and shedding, as well as the detectability of symptoms. We show that due to an early onset of infectiousness, which is reported to be synchronous or even precede the onset of detectable symptoms, the tracing and immediate testing of all who came in contact with the detected infected individual reduce the spread of epidemics, hospital load, and fatality rate. We also investigate how the strictness and promptness of the isolation of infected individuals affect the outcome of epidemics. We hope that these more precise node dynamics could be incorporated into complex large-scale epidemiological models to improve the accuracy and credibility of predictions.

q-bio.PE↗

arXiv2025

The number of immune defense and counter-defense systems sustained in the arms race between procaryotes and viruses

Prokaryotes have evolved various mechanisms to counter viruses, which in their turn developed numerous strategies to avoid defenses of the hosts. Dozens of such defense and counter-defense mechanisms have recently been discovered, yet the number of such systems held by a given virus or its host is limited. Here, we present numerical and theoretical arguments for the existence of the maximal number of ecologically and evolutionary sustainable defense and counter-defense systems maintained by both sides at any time of the never-ending evolutionary arms race. We find that the number of such systems is of the order of 10 for a broad range of assumptions about the costs and benefits of defense and counter-defense mechanisms and their specificity. This optimum in the number of defense and counter-defense systems appears as a result of a compromise between the metabolic and autoimmune costs of adding a new layer of defense and the benefits it conveys.

q-bio.PE↗

arXiv2023

On the evolutionary emergence of predation

In models for the evolution of predation from initially purely competitive species interactions, the propensity of predation is most often assumed to be a direct consequence of the relative morphological and physiological traits of interacting species. Here we explore a model in which predation ability is an independently evolving phenotypic feature, so that even when the relative morphological or physiological traits allow for predation, predation only occurs if the predation ability of individuals has independently evolved to high enough values. In addition to delineating the conditions for the evolutionary emergence of predation, the model reproduces stationary and non-stationary multilevel food webs with the top predators not necessarily having size superiority.

q-bio.PE↗

arXiv2017

Optimal number of spacers in CRISPR arrays

We estimate the number of spacers in a CRISPR array of a bacterium which maximizes its protection against a viral attack. The optimality follows from a competition between two trends: too few distinct spacers make the bacteria vulnerable to an attack by a virus with mutated corresponding protospacers, while an excessive variety of spacers dilutes the number of the CRISPR complexes armed with the most recent and thus most effective spacers. We first evaluate the optimal number of spacers in a simple scenario of an infection by a single viral species and later consider a more general case of multiple viral species. We find that depending on such parameters as the concentration of CRISPR-CAS interference complexes and its preference to arm with more recently acquired spacers, the rate of viral mutation, and the number of viral species, the predicted optimal array length lies within a range quite reasonable from the viewpoint of recent experiments.

q-bio.PE↗