Self-inhibiting percolation and viral spreading in epithelial tissue.

SARS-CoV-2 induces delayed type-I/III interferon production, allowing it to escape the early innate immune response. The delay has been attributed to a deficiency in the ability of cells to sense viral replication upon infection, which in turn hampers activation of the antiviral state in bystander cells. Here, we introduce a cellular automaton model to investigate the spatiotemporal spreading of viral infection as a function of virus and host-dependent parameters.

Diversity and ecotones in a model ecosystems of sessile species.

Sessile species compete for space and accessible light, with directed interactions evident in one species overgrowing another and with multispecies systems characterized by nontransitive relationships. Such patterns are observed in coral reefs or lichens on rock surfaces. Open systems with episodic invasions of such species have been predicted to exhibit a stable high-diversity state when the interaction probability is below a certain critical threshold.

The dynamics of phage predation on a microcolony.

Phage predation is an important factor for controlling the bacterial biomass. At face value, dense microbial habitats are expected to be vulnerable to phage epidemics due to the abundance of fresh hosts immediately next to any infected bacteria. Despite this, the bacterial microcolony is a common habitat for bacteria in nature.

The counterintuitive implications of superspreading diseases.

Superspreading is known to have played an important role in the transmission dynamics of SARS-CoV-2. In this Comment, the authors discuss how knowledge of the extent and cause of superspreading is important for designing appropriate control measures for emerging infectious diseases.

Epigenetic switching with asymmetric bridging interactions.

Gene expression states are often stably sustained in cis despite massively disruptive events like DNA replication. This is achieved by on-going enzymatic activity that maintains parts of the DNA in either heterochromatic (packed) or euchromatic (free) states, each of which is stabilized by both positive feedback and bridging interactions between individual nucleosomes. In contrast to condensed matter, however, the dynamics is not only governed by equilibrium binding interactions but is also mediated by enzymes that recognize and act on specific amino acid tails of the nucleosomes.

Host heterogeneity and epistasis explain punctuated evolution of SARS-CoV-2.

Identifying drivers of viral diversity is key to understanding the evolutionary as well as epidemiological dynamics of the COVID-19 pandemic. Using rich viral genomic data sets, we show that periods of steadily rising diversity have been punctuated by sudden, enormous increases followed by similarly abrupt collapses of diversity. We introduce a mechanistic model of saltational evolution with epistasis and demonstrate that these features parsimoniously account for the observed temporal dynamics of inter-genomic diversity.

Jag1-Notch cis-interaction determines cell fate segregation in pancreatic development.

The Notch ligands Jag1 and Dll1 guide differentiation of multipotent pancreatic progenitor cells (MPCs) into unipotent pro-acinar cells (PACs) and bipotent duct/endocrine progenitors (BPs). Ligand-mediated trans-activation of Notch receptors induces oscillating expression of the transcription factor Hes1, while ligand-receptor cis-interaction indirectly represses Hes1 activation. Despite Dll1 and Jag1 both displaying cis- and trans-interactions, the two mutants have different phenotypes for reasons not fully understood.

Emerging diversity in a population of evolving intransitive dice.

Exploiting the mathematical curiosity of intransitive dice, we present a simple theoretical model for coevolution that captures scales ranging from the genome of the individual to the system-wide emergence of species diversity. We study a set of evolving agents that interact competitively in a closed system, in which both the dynamics of mutations and competitive advantage emerge directly from interpreting a genome as the sides of a die. The model demonstrates sympatric speciation where new species evolve from existing ones while in contact with the entire ecosystem.

Emergence of networks of shared restriction-modification systems in phage-bacteria ecosystems.

Restriction-modification (RM) systems are the most ubiquitous bacterial defence systems against bacteriophages. Using genome sequence data, we showed that RM systems are often shared among bacterial strains in a structured way. Examining the network of interconnections between bacterial strains within genera, we found that many strains share more RM systems than expected compared with a suitable null model.

Immune Heterogeneity and Epistasis Explain Punctuated Evolution of SARS-CoV-2.

Identifying drivers of viral diversity is key to understanding the evolutionary as well as epidemiological dynamics of the COVID-19 pandemic. Using rich viral genomic data sets, we show that periods of steadily rising diversity have been punctuated by sudden, enormous increases followed by similarly abrupt collapses of diversity. We introduce a mechanistic model of saltational evolution with epistasis and demonstrate that these features parsimoniously account for the observed temporal dynamics of inter-genomic diversity.

Lockdowns exert selection pressure on overdispersion of SARS-CoV-2 variants.

The SARS-CoV-2 ancestral strain has caused pronounced superspreading events, reflecting a disease characterized by overdispersion, where about 10% of infected people cause 80% of infections. New variants of the disease have different person-to-person variability in viral load, suggesting for example that the Alpha (B.1.

From kill the winner to eliminate the winner in open phage-bacteria systems.

Phages and bacteria manage to coexist and sustain ecosystems with a high diversity of strains, despite limited resources and heavy predation. This diversity can be explained by the "kill the winner" model where virulent phages predominantly prey on fast-growing bacteria and thereby suppress the competitive exclusion of slower-growing bacteria. Here we computationally investigate the robustness of these systems against invasions, where new phages or bacteria may interact with more than one of the resident strains.

The transcription factor Atf1 lowers the transition barrier for nucleosome-mediated establishment of heterochromatin.

Transcription factors can exert opposite effects depending on the chromosomal context. The fission yeast transcription factor Atf1 both activates numerous genes in response to stresses and mediates heterochromatic gene silencing in the mating-type region. Investigating this context dependency, we report here that the establishment of silent heterochromatin in the mating-type region occurs at a reduced rate in the absence of Atf1 binding.

Protection of bacteriophage-sensitive by lysogens.

SignificanceSome viruses that infect bacteria, temperate bacteriophages, can confer immunity to infection by the same virus. Here we report -immune bacteria could protect -sensitive bacteria from killing by phage in mixed culture. The protection depended on the extent to which the immune bacteria were able to adsorb the phage.

Spatial model of Ebola outbreaks contained by behavior change.

The West African Ebola (2014-2016) epidemic caused an estimated 11.310 deaths and massive social and economic disruption. The epidemic was comprised of many local outbreaks of varying sizes.

Superspreading quantified from bursty epidemic trajectories.

The quantification of spreading heterogeneity in the COVID-19 epidemic is crucial as it affects the choice of efficient mitigating strategies irrespective of whether its origin is biological or social. We present a method to deduce temporal and individual variations in the basic reproduction number directly from epidemic trajectories at a community level. Using epidemic data from the 98 districts in Denmark we estimate an overdispersion factor k for COVID-19 to be about 0.

Differences in social activity increase efficiency of contact tracing.

Abstract: Digital contact tracing has been suggested as an effective strategy for controlling an epidemic without severely limiting personal mobility. Here, we use smartphone proximity data to explore how social structure affects contact tracing of COVID-19. We model the spread of COVID-19 and find that the effectiveness of contact tracing depends strongly on social network structure and heterogeneous social activity.

Superspreading of airborne pathogens in a heterogeneous world.

Epidemics are regularly associated with reports of superspreading: single individuals infecting many others. How do we determine if such events are due to people inherently being biological superspreaders or simply due to random chance? We present an analytically solvable model for airborne diseases which reveal the spreading statistics of epidemics in socio-spatial heterogeneous spaces and provide a baseline to which data may be compared. In contrast to classical SIR models, we explicitly model social events where airborne pathogen transmission allows a single individual to infect many simultaneously, a key feature that generates distinctive output statistics.

The COVID-19 pandemic: key considerations for the epidemic and its control.

The response to the ongoing COVID-19 pandemic has been characterized by draconian measures and far too many important unknowns, such as the true mortality risk, the role of children as transmitters and the development and duration of immunity in the population. More than a year into the pandemic much has been learned and insights into this novel type of pandemic and options for control are shaping up. Using a historical lens, we review what we know and still do not know about the ongoing COVID-19 pandemic.

Establishment of heterochromatin in domain-size-dependent bursts.

Methylation of histone H3K9 is a hallmark of epigenetic silencing in eukaryotes. Nucleosome modifications often rely on positive feedback where enzymes are recruited by modified nucleosomes. A combination of local and global feedbacks has been proposed to account for some dynamic properties of heterochromatin, but the range at which the global feedbacks operate and the exact mode of heterochromatin propagation are not known.

COVID-19 Superspreading Suggests Mitigation by Social Network Modulation.

Although COVID-19 has caused severe suffering globally, the efficacy of nonpharmaceutical interventions has been greater than typical models have predicted. Meanwhile, evidence is mounting that the pandemic is characterized by superspreading. Capturing this phenomenon theoretically requires modeling at the scale of individuals.

Overdispersion in COVID-19 increases the effectiveness of limiting nonrepetitive contacts for transmission control.

Increasing evidence indicates that superspreading plays a dominant role in COVID-19 transmission. Recent estimates suggest that the dispersion parameter for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is on the order of 0.1, which corresponds to about 10% of cases being the source of 80% of infections.

Social contagion in a world with asymmetric influence.

Social media has blurred the distinction between news outlets and social networks by giving everyone access to mass communication. We simulate how influencers compete for attention on a social network by spreading information. The network structure occupies an ordered metastable state where one influencer maintains dominance for a sustained period or a fragmented state that divides attention between influencers.

SARS-CoV-2 superspreading in cities vs the countryside.

The first wave of the COVID-19 pandemic was characterized by an initial rapid rise in new cases followed by a peak and a more erratic behaviour that varies between regions. This is not easy to reproduce with traditional SIR models, which predict a more symmetric epidemic. Here, we argue that superspreaders and population heterogeneity would predict such behaviour even in the absence of restrictions on social life.

Cost-benefit of limited isolation and testing in COVID-19 mitigation.

The international community has been put in an unprecedented situation by the COVID-19 pandemic. Creating models to describe and quantify alternative mitigation strategies becomes increasingly urgent. In this study, we propose an agent-based model of disease transmission in a society divided into closely connected families, workplaces, and social groups.