On a bi-virus epidemic model with partial and waning immunity

We propose a deterministic compartmental model to study the impact of partial and waning immunity on the spread of two competitive epidemic diseases, hereafter termed viruses. Building on a standard bi-virus SIS model, we introduce additional compartments to account for individuals who recovered from each virus, and tunable parameters to capture the level of virus-specific and cross protection acquired after recovery from a specific virus, and the rate at which such immunity could wane. We formalise the model as a system of nonlinear ordinary differential equations, which is amenable to analytical treatment, and we focus our analysis on two specialisations of the model. First, in the absence of waning immunity, we establish a global convergence result showing that, above the epidemic threshold, only the “fittest” virus becomes endemic. Second, in the absence of cross-immunity, we demonstrate instead that long-lasting co-existence of the two viruses may emerge, depending on the model parameters

Graph Theory and Networks in Biology

In this paper, we present a survey of the use of graph theoretical techniques in Biology. In particular, we discuss recent work on identifying and modelling the structure of bio-molecular networks, as well as the application of centrality measures to interaction networks and research on the hierarchical structure of such networks and network motifs. Work on the link between structural network properties and dynamics is also described, with emphasis on synchronization and disease propagation.Comment: 52 pages, 5 figures, Survey Pape

Phylodynamic theory of persistence, extinction and speciation of rapidly adapting pathogens

Rapidly evolving pathogens like influenza viruses can persist by changing their antigenic properties fast enough to evade the adaptive immunity, yet they rarely split into diverging lineages. By mapping the multi-strain Susceptible-Infected-Recovered model onto the traveling wave model of adapting populations, we demonstrate that persistence of a rapidly evolving, Red-Queen-like state of the pathogen population requires long-ranged cross-immunity and sufficiently large population sizes. This state is unstable and the population goes extinct or 'speciates' into two pathogen strains with antigenic divergence beyond the range of cross-inhibition. However, in a certain range of evolutionary parameters, a single cross-inhibiting population can exist for times long compared to the time to the most recent common ancestor ([Formula: see text]) and gives rise to phylogenetic patterns typical of influenza virus. We demonstrate that the rate of speciation is related to fluctuations of [Formula: see text] and construct a 'phase diagram' identifying different phylodynamic regimes as a function of evolutionary parameters

Unveiling Human Non-Random Genome Editing Mechanisms Activated in Response to Chronic Environmental Changes: I. Where Might These Mechanisms Come from and What Might They Have Led To?

none1noThis article challenges the notion of the randomness of mutations in eukaryotic cells by unveiling stress-induced human non-random genome editing mechanisms. To account for the existence of such mechanisms, I have developed molecular concepts of the cell environment and cell environmental stressors and, making use of a large quantity of published data, hypothesised the origin of some crucial biological leaps along the evolutionary path of life on Earth under the pressure of natural selection, in particular, (1) virus-cell mating as a primordial form of sexual recombination and symbiosis; (2) Lamarckian CRISPR-Cas systems; (3) eukaryotic gene development; (4) antiviral activity of retrotransposon-guided mutagenic enzymes; and finally, (5) the exaptation of antiviral mutagenic mechanisms to stress-induced genome editing mechanisms directed at "hyper-transcribed" endogenous genes. Genes transcribed at their maximum rate (hyper-transcribed), yet still unable to meet new chronic environmental demands generated by "pollution", are inadequate and generate more and more intronic retrotransposon transcripts. In this scenario, RNA-guided mutagenic enzymes (e.g., Apolipoprotein B mRNA editing catalytic polypeptide-like enzymes, APOBECs), which have been shown to bind to retrotransposon RNA-repetitive sequences, would be surgically targeted by intronic retrotransposons on opened chromatin regions of the same "hyper-transcribed" genes. RNA-guided mutagenic enzymes may therefore "Lamarkianly" generate single nucleotide polymorphisms (SNP) and gene copy number variations (CNV), as well as transposon transposition and chromosomal translocations in the restricted areas of hyper-functional and inadequate genes, leaving intact the rest of the genome. CNV and SNP of hyper-transcribed genes may allow cells to surgically explore a new fitness scenario, which increases their adaptability to stressful environmental conditions. Like the mechanisms of immunoglobulin somatic hypermutation, non-random genome editing mechanisms may generate several cell mutants, and those codifying for the most environmentally adequate proteins would have a survival advantage and would therefore be Darwinianly selected. Non-random genome editing mechanisms represent tools of evolvability leading to organismal adaptation including transgenerational non-Mendelian gene transmission or to death of environmentally inadequate genomes. They are a link between environmental changes and biological novelty and plasticity, finally providing a molecular basis to reconcile gene-centred and "ecological" views of evolution.openZamai, LorisZamai, Lori

A survey on the analysis and control of evolutionary matrix games

In support of the growing interest in how to efficiently influence complex systems of interacting self interested agents, we present this review of fundamental concepts, emerging research, and open problems related to the analysis and control of evolutionary matrix games, with particular emphasis on applications in social, economic, and biological networks. (C) 2018 Elsevier Ltd. All rights reserved