Bulletin of the American Physical Society
APS March Meeting 2023
Volume 68, Number 3
Las Vegas, Nevada (March 5-10)
Virtual (March 20-22); Time Zone: Pacific Time
Session Z08: Evolutionary Dynamics IIFocus
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Sponsoring Units: DBIO Chair: Antonio Carlos Costa, Ecole Normale Superieure Paris Room: Room 131 |
Friday, March 10, 2023 11:30AM - 12:06PM |
Z08.00001: Ivana Cvijovic Invited Speaker: Ivana Cvijovic
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Friday, March 10, 2023 12:06PM - 12:18PM |
Z08.00002: Evaluating the Logic of Selection in Germinal Centers Bertrand J Ottino-Loffler, Gabriel Victora A central feature of vertebrate immune response is affinity maturation, wherein antibody-producing B cells undergo evolutionary selection in substructures of lymph nodes, called germinal centers. While it has been shown that the median B cell affinity dependably increases over the course of maturation, the exact logic behind this evolution remains vague. Three simple, potential selection methods include encouraging the reproduction of high affinity cells (“birth selection”), encouraging cell death in low affinity cells (“death selection”), and adjusting the mutation rate based on cell affinity (“mutational selection”). While all three forms of selection would lead to a net increase in affinity, different selection methods lead to distinct statistical dynamics. We discuss ramifications of different evolutionary models, and encourage thinking about evolutionary fitness as more than a singular number. |
Friday, March 10, 2023 12:18PM - 12:30PM |
Z08.00003: Lineage frequency fluctuations reveal the spatial dynamics of disease transmission in SARS-CoV-2 Takashi Okada, Giulio Isacchini, QinQin Yu, Oskar Hallatschek Human mobility is a key factor in the spatial transmission of infectious diseases. Although human mobility can be quantified from survey data or cell phone data, it remains difficult to generate reliable models of the spatial-transmission dynamics from mobility data due to the complexity of the underlying epidemiological processes. For SARS-COV-2, a vast amount of lineage data is available with unprecedented spatio-temporal resolution. Here, we develop a data-driven method that uses time series neutral lineage frequencies data to infer an infectivity matrix, which describes the transmission rates between individuals in different locations. From the inferred infectivity matrix, we can determine epidemiologically relevant quantities, such as the relaxation timescale of the dynamics, the dispersal kernel associated with the disease transmission, and the spatial-spreading pattern of a new variant. Our method is also applicable to infer the couplings between non-spatial groups, such as age groups, where mobility proxies are unavailable. |
Friday, March 10, 2023 12:30PM - 12:42PM |
Z08.00004: Comparative efficacy of antiviral strategies targeting different stages of the viral life cycle: A viral quasispecies dynamics study Pancy Lwin, Greyson R Lewis, Moumita Das, Barbara Jones While the COVID-19 pandemic continues, the use of antivirals provides hope for preventing and mitigating similar viral outbreaks. What is the comparative impact of different antiviral therapeutics? How do antivirals impact the viral load, i.e., the virus population in an individual’s bloodstream, in high and low-immunity individuals? We use a model of viral quasispecies dynamics to examine the efficacy of antiviral strategies targeting three critical aspects of the viral life cycle: fecundity, reproduction rate, or infection rate in individuals with varying degree of immunity [1]. We find a linear relationship between the viral load with the change in fecundity and a power law relationship with the change in the reproduction rate of the virus, with the viral load decreasing as the fecundity and the reproduction rates are decreased. Interestingly, however, for antivirals that target the infection rate, the viral load changes non-monotonically; the viral population initially increases and then decreases as the infection rate is decreased. The initial increase is especially pronounced for individuals with low immunity. We found that the therapeutics are only effective in such individuals if they stop the infection process entirely. Our results predict the effectiveness of different antiviral strategies for COVID-19 and similar viral diseases and provide insights into the susceptibility of individuals with low immunity to effects like long covid. |
Friday, March 10, 2023 12:42PM - 12:54PM |
Z08.00005: The dynamics of LINE-1 retrotransposition in cellular populations Stephen Martis, Alexander Solovyov, Jayon Lihm, Hao Li, Benjamin Greenbaum Retrotransposons are genetic elements that have the ability to copy and paste themselves in the genome via the proteins they encode. Since the rapid growth of a retrotransposon can be highly deleterious at the organismal level, many of these genetic parasites are suppressed or have been inactivated over evolutionary time. However, the human genome still hosts the active retrotransposon LINE-1, whose aberrant expression is associated with disease, ranging from neurological disorders to cancer. Despite these associations, a quantitative understanding of the dynamics and diversity of LINE-1 insertions in somatic tissue is lacking. In order to address this gap, we present a population dynamic model of LINE-1 retrotransposition in individual cells. Using the model, we show that at demographic equilibrium, the LINE-1 copy number distribution is broader than would be expected from classical population genetic models. We demonstrate how this broadening distorts the frequency spectrum of insertions. We compare the model's predictions to data from whole genome sequencing of individual tumor cells. |
Friday, March 10, 2023 12:54PM - 1:06PM |
Z08.00006: Influence of cross immunoreactive network topology and internal dynamics of the immune system on antigenic cooperation Kevin Ng Chau, Jason T George, Herbert Levine The recent discovery of antigenic cooperation (AC) provides an explanation for the persistence of viral strains in the host during chronic infection (like in hepatitis C virus) that better fits the experimental evidence when compared to the immune-escape hypothesis. As it is currently understood, AC leverages altruistic strains of the virus that sacrifice their own fitness through immunodominance to benefit persistent strains. This dynamic leaves sections of the cross immunoreactivity network (CRN) invisible to the host’s immune system, with persistent strains located in such invisible sections, a phenomenon known as local immunodeficiency (LI). However, all the efforts so far have focused on the interacting dynamics of the viral strains with the entire immune response accounted as a whole. It remains unclear whether the LI emerges solely from the topology of the CRN or if the intricate inner functioning of the immune system has a significant contribution. We investigate these inquiries on LI by fine-graining the immune system dynamics and by exploring the influence of network topology on AC. Our modeling approach is broadly applicable to understanding the internal dependencies of cooperation on internal dynamics of distinct immune features, along with their role in autoimmune and chronic disease |
Friday, March 10, 2023 1:06PM - 1:18PM |
Z08.00007: Eco-evolutionary stable strategies of antigenically escaping viruses Victor Chardès, Andrea Mazzolini, Aleksandra M Walczak, Thierry Mora Antigenic variation is the main immune escape mechanism for RNA viruses like influenza or SARS-CoV-2, promoting diversity in the viral population and leading to repeated epidemics and reinfections. This antigenic evolution is sustained by continuous pathogen transmission between hosts and is fueled by remarkably high viral mutation rates. While high mutation rates clearly promote antigenic escape, they also induce a large mutational load, reducing viral fitness. In this context, it remains unclear how the immune pressure exerted by a population of hosts drives the evolution of these viral strategies. To tackle this question we model the co-evolution between finite population of hosts and viruses in a one dimensional antigenic space whose metric describes the cross-reactivity between viral variants and antibodies generated by previous infections. We observe that the antigenic evolution induced by the immune pressure is characterized by a traveling wave of adaptation whose speed and size are primarily ruled by the efficiency of cross-reactive immunity. As a consequence, we show that the evolutionary stable viral strategy is dictated by a trade-off between maximizing the speed of antigenic evolution when the cross-reactivity is small and maximizing the reproduction ratio when it is larger. In particular, this result implies that a small cross-reactivity favors the evolution of highly transmissible and deadly viruses with mutation rates close to the extinction threshold. |
Friday, March 10, 2023 1:18PM - 1:30PM |
Z08.00008: Spatiotemporal population dynamics of native and engineered bacteria in the gut microbiome Alberto Alonso, Moumita Das Colorectal (CRC) cancer is the fourth most commonly diagnosed cancer and the fourth most common cause of cancer deaths in the US. Recent studies have indicated a rise in CRC in adults under fifty, a subset of the population that does not undergo regular screening for CRC. Recent research shows that the gut microbiome plays an important role in CRC. We are part of a collaborative team of experimentalists and modelers developing a non-invasive approach where genetically modified native bacteria in the gut microbiome can be used to diagnose and disrupt CRC. As part of the theory and modeling, we use a generalized model of population dynamics that extends the Lotka-Volterra equations beyond the usual predator-prey dynamics to include other types of interactions between engineered and native bacterial species. We also include bacteria's diffusion and advection to account for the spatial movement and variation of different bacterial populations. By solving the resulting spatiotemporal population dynamics, we make predictions of the conditions for the survival and grafting of engineered bacterial populations in the gut microbiome. Our results also provide an understanding of how different types of microbial interactions impact the dynamics of these bacterial populations. |
Friday, March 10, 2023 1:30PM - 1:42PM |
Z08.00009: Tuning spatial distributions of selection pressure to suppress emergence of resistance Thomas Tunstall, Philip Madgwick, Ricardo Kanitz, Wolfram Moebius Combatting pathogenic bacteria with antibiotics, pests with pesticides, and tumours with cancer drugs all prompt an evolutionary response: the emergence of resistance to the control agent, i.e., the selection pressure, meant to control the population. What measures can be taken to suppress the emergence of resistance while not foregoing the benefits of population control? More specifically, we here ask whether the selection pressure can be applied in a way that minimises the rise of an existing resistant subpopulation. |
Friday, March 10, 2023 1:42PM - 1:54PM |
Z08.00010: Heterogeneity in bacterial filamentation survival dynamics decrease in response to increased stress Robert H Austin, Julia Bos, George Butler, Kenneth J Pienta, Sarah Amend The evolution of antibiotic resistance is a fundamental and lethal problem in disease management. Yet, while phenotypic diversity serves as the substrate for adaptation to emerge, including resistance, it is rarely quantified on a single cell level. Through the use of a novel dual reporter strain of E. coli we show that increased survival is correlated with continued DNA replication at both moderate and high levels of ciprofloxacin treatment but that the heterogeneity in response is increased at the lower treatment level. Similarly, we show that the survival time is also increased through a reduction in the abundance of misfolded proteins but that the mechanism of misfolded protein reduction is dependent on the treatment level. Taken as a whole, our results show the diverse range of survival tactics that are employed by cells in response to stress and highlight the power of single cell phenotyping in revealing potential evolutionary routes to resistance. |
Friday, March 10, 2023 1:54PM - 2:06PM |
Z08.00011: Dynamic trait shift and its effects on biological populations Zachary L Jackson, BingKan Xue A biological population exhibits a distribution of traits among individuals that affect how they interact with other species and the environment. This distribution of trait values can shift under three types of influences: differential growth, phenotypic plasticity, and preferential consumption by the predator. Ecological models of population dynamics and species distributions often focus on "density effects", ignoring trait shifts. Through a simple predator-prey model that explicitly tracks the trait distribution of the prey, we explore the implications of trait shifts. We quantify "trait effects" resulting from the shift in trait distribution, first on the prey population itself, including the healthy herd effect and emergent promotion. We then show the back-reaction on the predator, which may reduce its population and possibly even result in its extinction. Our results suggest that including trait shifts in modeling ecological dynamics will be important for predicting species interactions and persistence. |
Friday, March 10, 2023 2:06PM - 2:18PM |
Z08.00012: Commuter interactions shape disease spread Aaron C Winn, Eleni Katifori Interactions between commuting individuals can lead to large-scale spreading of rumors, ideas, or disease, even though the commuters have no eventual net displacement. The emergent dynamics depend crucially on the commuting distribution of a population, that is how the probability to travel to a destination decays with distance from home. Applying this idea to epidemics, we will demonstrate the qualitatively different infection dynamics emerging from populations with different commuting distributions. If the commuting distribution is highly localized, we recover a reaction-diffusion system and observe Fisher waves traveling at a speed proportional to the characteristic commuting distance. If the commuting distribution has a long tail, then no finite-velocity Fisher waves can form, but we show that, in some regimes, there is nontrivial spatial dependence that the well-mixed approximation neglects. We discuss how, in all cases, an initial spreading-dominated regime can allow the disease to go undetected for a finite amount of time before exponential growth takes over. This "offset time" is a quantity of huge importance for epidemic surveillance and yet largely ignored in the literature. |
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