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We provide quantitative estimates on the size and the structure of the epistatic space defined in the main article, Dynamical Correlations in the escape strategy of Influenza A virus, EPL 101 68003.
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So far most of the analysis of coronavirus 2020 epidemic data has been focusing on a short-time window and consequently a quantitative test of statistical physical laws of Coronavirus Epidemics with Containment Measures (CEwCM) is currently lacking. Here we report a quantitative analysis of CEwCM over 230 days, covering the full-time lapse of the first epidemic wave. We use a 3D phase diagram tracking the simultaneous evolution of the doubling time Td(t) and reproductive number Rt(t) showing that this expanded parameter space is needed for biological physics of CEwCP. We have verified that in the supercritical [Rt(t)>1, Td(t)<40 days] regime i) the curve Z(t) of total infected cases follows the growth rate called Ostwald law; ii) the doubling time follows the exponential law Td(t)=A exp((t-t0)/s) as a function of time and iii) the power law Td(t)=C(Rt(t)-1)^-n is verified with the exponent n depending on the definition of Rt(t). The log-log plots Td(t) versus (Rt-1) of the second 2020 epidemic wave unveil in the subcritical regime [Td(t)>100 days] arrested metastable phases with Rt>1 where Td(t) was kept constant followed by its explosion and its containment following the same power law as in the first wave
A tragedy of the commons (TOC) occurs when individuals acting in their own self-interest deplete commonly-held resources, leading to a worse outcome than had they cooperated. Over time, the depletion of resources can change incentives for subsequent actions. Here, we investigate long-term feedback between game and environment across a continuum of incentives in an individual-based framework. We identify payoff-dependent transition rules that lead to oscillatory TOC-s in stochastic simulations and the mean field limit. Further extending the stochastic model, we find that spatially explicit interactions can lead to emergent, localized dynamics, including the propagation of cooperative wave fronts and cluster formation of both social context and resources. These dynamics suggest new mechanisms underlying how TOCs arise and how they might be averted.
Understanding how genotypes map onto phenotypes, fitness, and eventually organisms is arguably the next major missing piece in a fully predictive theory of evolution. We refer to this generally as the problem of the genotype-phenotype map. Though we are still far from achieving a complete picture of these relationships, our current understanding of simpler questions, such as the structure induced in the space of genotypes by sequences mapped to molecular structures, has revealed important facts that deeply affect the dynamical description of evolutionary processes. Empirical evidence supporting the fundamental relevance of features such as phenotypic bias is mounting as well, while the synthesis of conceptual and experimental progress leads to questioning current assumptions on the nature of evolutionary dynamics-cancer progression models or synthetic biology approaches being notable examples. This work delves into a critical and constructive attitude in our current knowledge of how genotypes map onto molecular phenotypes and organismal functions, and discusses theoretical and empirical avenues to broaden and improve this comprehension. As a final goal, this community should aim at deriving an updated picture of evolutionary processes soundly relying on the structural properties of genotype spaces, as revealed by modern techniques of molecular and functional analysis.
Eigens quasi-species model describes viruses as ensembles of different mutants of a high fitness master genotype. Mutants are assumed to have lower fitness than the master type, yet they coexist with it forming the quasi-species. When the mutation rate is sufficiently high, the master type no longer survives and gets replaced by a wide range of mutant types, thus destroying the quasi-species. It is the so-called error catastrophe. But natural selection acts on phenotypes, not genotypes, and huge amounts of genotypes yield the same phenotype. An important consequence of this is the appearance of beneficial mutations which increase the fitness of mutants. A model has been recently proposed to describe quasi-species in the presence of beneficial mutations. This model lacks the error catastrophe of Eigens model and predicts a steady state in which the viral population grows exponentially. Extinction can only occur if the infectivity of the quasi-species is so low that this exponential is negative. In this work I investigate the transient of this model when infection is started from a small amount of low fitness virions. I prove that, beyond an initial regime where viral population decreases (and can go extinct), the growth of the population is super-exponential. Hence this population quickly becomes so huge that selection due to lack of host cells to be infected begins to act before the steady state is reached. This result suggests that viral infection may widespread before the virus has developed its optimal form.
In this research, methods and computational results based on statistical analysis and mathematical modelling, data collection in situ in order to make a hazard map of Hanta Virus infection in the region of Araucania, Chile are presented. The development of this work involves several elements such as Landsat satellite images, biological information regarding seropositivity of Hanta Virus and information concerning positive cases of infection detected in the region. All this information has been processed to find a function that models the danger of contagion in the region, through logistic regression analysis and Artificial Neural Networks
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