Pub Date : 2025-12-18DOI: 10.1016/j.jtbi.2025.112334
Rahnuma Islam, Bard Ermentrout, Sabrina Streipert
We introduce a discrete-time continuous-space neural model to produce diverse shell structures and pigmentation patterns observed in aquatic mollusks. The model builds on an earlier neural model for shell patterns by incorporating the inhibition as a separate population and thus eliminates the need for a “refractory” substance, yet is still able to produce many varieties of molluscan pigmentation patterns. The model utilizes a system of neural excitation and inhibition to conduct secretory activity and successfully replicates various natural shell patterns found in these organisms. Through an analysis of local stability around equilibria and an analysis of bifurcation, we establish the critical role of parameters involved in our system on the bifurcations in governing the emergence of spatial, temporal, and spatio-temporal patterns.
{"title":"A discrete-time continuous-space neural model for shell patterns in mollusks","authors":"Rahnuma Islam, Bard Ermentrout, Sabrina Streipert","doi":"10.1016/j.jtbi.2025.112334","DOIUrl":"10.1016/j.jtbi.2025.112334","url":null,"abstract":"<div><div>We introduce a discrete-time continuous-space neural model to produce diverse shell structures and pigmentation patterns observed in aquatic mollusks. The model builds on an earlier neural model for shell patterns by incorporating the inhibition as a separate population and thus eliminates the need for a “refractory” substance, yet is still able to produce many varieties of molluscan pigmentation patterns. The model utilizes a system of neural excitation and inhibition to conduct secretory activity and successfully replicates various natural shell patterns found in these organisms. Through an analysis of local stability around equilibria and an analysis of bifurcation, we establish the critical role of parameters involved in our system on the bifurcations in governing the emergence of spatial, temporal, and spatio-temporal patterns.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"620 ","pages":"Article 112334"},"PeriodicalIF":2.0,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145800907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-17DOI: 10.1016/j.jtbi.2025.112354
Bivash Kaity , Daniel Lobo
The development and regeneration of multicellular organisms require dynamic coordination between cellular behaviors and mechanochemical signals to achieve precise and stable tissue shapes. Plastic organisms, such as planarians, can regenerate, grow, and degrow as adults while maintaining precise whole-body and organ tissue shapes. However, the mechanisms underlying the pathways that coordinate and integrate these signals into the correct balance between cellular growth, mitosis, and apoptosis to form emergent target tissue shapes remain poorly understood. Here, we present a systematic theoretical study of the biological drivers controlling the feedback mechanisms between tissue growth and morphogen signaling. The approach is based on lattice-free, center-based simulations of cell size dynamics, mitosis, and apoptosis governed by both intercellular diffusible morphogen concentrations and mechanical stress between cells to drive their spatial organization. The results demonstrate how different morphogen properties and tissue mechanics form a feedback loop that is essential for the robust regulation of target tissue shapes. Furthermore, we show that stable tissue shapes can emerge and regenerate from self-regulated patterning processes, such as Turing systems, controlling cellular growth dynamics. A stable feedback loop can form between the emergent morphogen patterns and the dynamics of cellular growth they regulate, as the tissue dynamics define the domain in which morphogens diffuse and hence pattern. Overall, this study highlights the essential role of the feedback loop between morphogen patterning and cellular growth in the regulation of tissue dynamics for stable shape formation. Moreover, this work establishes a framework for further experiments to understand the regulatory dynamics of whole-body development and regeneration using models with high spatiotemporal resolution.
Significance
Tight coordination and interpretation of the multitude of signals at different biological scales– from intracellular signals to mechanical interactions–are essential during the development and regeneration of multicellular organisms. In this work, we investigate the leading role of the feedback between mechanochemical signaling networks and tissue shape through cellular behaviors such as growth, proliferation, and apoptosis. This study demonstrates the interdependence between tissue growth and pattern formation mechanisms in the regulation of stable tissue shapes. Overall, this research provides novel mechanistic insights into the formation of tissue shapes through the regulatory feedback interaction between cell growth and patterning dynamics.
{"title":"Emergent stable tissue shapes from the regulatory feedback between morphogens and cell growth","authors":"Bivash Kaity , Daniel Lobo","doi":"10.1016/j.jtbi.2025.112354","DOIUrl":"10.1016/j.jtbi.2025.112354","url":null,"abstract":"<div><div>The development and regeneration of multicellular organisms require dynamic coordination between cellular behaviors and mechanochemical signals to achieve precise and stable tissue shapes. Plastic organisms, such as planarians, can regenerate, grow, and degrow as adults while maintaining precise whole-body and organ tissue shapes. However, the mechanisms underlying the pathways that coordinate and integrate these signals into the correct balance between cellular growth, mitosis, and apoptosis to form emergent target tissue shapes remain poorly understood. Here, we present a systematic theoretical study of the biological drivers controlling the feedback mechanisms between tissue growth and morphogen signaling. The approach is based on lattice-free, center-based simulations of cell size dynamics, mitosis, and apoptosis governed by both intercellular diffusible morphogen concentrations and mechanical stress between cells to drive their spatial organization. The results demonstrate how different morphogen properties and tissue mechanics form a feedback loop that is essential for the robust regulation of target tissue shapes. Furthermore, we show that stable tissue shapes can emerge and regenerate from self-regulated patterning processes, such as Turing systems, controlling cellular growth dynamics. A stable feedback loop can form between the emergent morphogen patterns and the dynamics of cellular growth they regulate, as the tissue dynamics define the domain in which morphogens diffuse and hence pattern. Overall, this study highlights the essential role of the feedback loop between morphogen patterning and cellular growth in the regulation of tissue dynamics for stable shape formation. Moreover, this work establishes a framework for further experiments to understand the regulatory dynamics of whole-body development and regeneration using models with high spatiotemporal resolution.</div></div><div><h3>Significance</h3><div>Tight coordination and interpretation of the multitude of signals at different biological scales– from intracellular signals to mechanical interactions–are essential during the development and regeneration of multicellular organisms. In this work, we investigate the leading role of the feedback between mechanochemical signaling networks and tissue shape through cellular behaviors such as growth, proliferation, and apoptosis. This study demonstrates the interdependence between tissue growth and pattern formation mechanisms in the regulation of stable tissue shapes. Overall, this research provides novel mechanistic insights into the formation of tissue shapes through the regulatory feedback interaction between cell growth and patterning dynamics.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"620 ","pages":"Article 112354"},"PeriodicalIF":2.0,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145792297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-17DOI: 10.1016/j.jtbi.2025.112350
Reinhard Blickhan , Tobias Siebert , Tom Weihmann
Hemolymph channels (lacunae) in the legs of spiders are part of their open circulatory system. They are defined as hemolymph-filled spaces between tissues within the exoskeletal tubes of the legs which are otherwise largely filled with muscles. In two of the major leg joints, the leg segments are connected via hinge joints with axes that are located at their dorsal rims.
The lacunae are used to channel hemolymph, which acts as a hydraulic fluid, to the extensor-less joints during the extension of the legs. However, due to competing optimization criteria of muscle-driven flexion and drainage of the hemolymph, fluid drag in the lacunae may hinder movement and force generation during flexion. Numerical modelling of dynamic flexions of the tibia-metatarsus joint, considering anatomical and physiological properties identified in the hunting spider Cupiennius salei, was used to investigate the trade-off between muscular force and hemolymph-drainage. The results showed that the diameters of the hemolymph channels exhibit a broad optimum for quick flexion. Within a wide range of channel diameters flexion times are hardly affected. Muscle properties, especially the time of muscle activation, strongly dampen the effect of the reduced muscle cross-section available. With small loads of 0.1g, similar to the spiders’ common prey size, the radius of the observed effective lacunae seems to enable the fastest flexions. A change in the aspect ratio of the tibia while maintaining the proportionality of its radius and the radius of the effective hemolymph channels leads to an extension of the flexion time.
{"title":"Semi-hydraulic actuation in spider legs: The transport of the hemolymph does not hamper muscle driven leg joint flexion","authors":"Reinhard Blickhan , Tobias Siebert , Tom Weihmann","doi":"10.1016/j.jtbi.2025.112350","DOIUrl":"10.1016/j.jtbi.2025.112350","url":null,"abstract":"<div><div>Hemolymph channels (lacunae) in the legs of spiders are part of their open circulatory system. They are defined as hemolymph-filled spaces between tissues within the exoskeletal tubes of the legs which are otherwise largely filled with muscles. In two of the major leg joints, the leg segments are connected via hinge joints with axes that are located at their dorsal rims.</div><div>The lacunae are used to channel hemolymph, which acts as a hydraulic fluid, to the extensor-less joints during the extension of the legs. However, due to competing optimization criteria of muscle-driven flexion and drainage of the hemolymph, fluid drag in the lacunae may hinder movement and force generation during flexion. Numerical modelling of dynamic flexions of the tibia-metatarsus joint, considering anatomical and physiological properties identified in the hunting spider <em>Cupiennius salei</em>, was used to investigate the trade-off between muscular force and hemolymph-drainage. The results showed that the diameters of the hemolymph channels exhibit a broad optimum for quick flexion. Within a wide range of channel diameters flexion times are hardly affected. Muscle properties, especially the time of muscle activation, strongly dampen the effect of the reduced muscle cross-section available. With small loads of 0.1g, similar to the spiders’ common prey size, the radius of the observed effective lacunae seems to enable the fastest flexions. A change in the aspect ratio of the tibia while maintaining the proportionality of its radius and the radius of the effective hemolymph channels leads to an extension of the flexion time.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"620 ","pages":"Article 112350"},"PeriodicalIF":2.0,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145792296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-13DOI: 10.1016/j.jtbi.2025.112344
Ruslan M. Timchenko , Mikhail A. Panteleev
The intrinsic pathway of apoptosis mediates programmed cell death in several major scenarios, but mechanisms regulating its triggering remain unclear. We developed a kinetic mathematical model based on ordinary differential equations and the law of mass action to investigate whether bistability in the regulatory system of the intrinsic apoptotic pathway can be achieved purely on the basis of Bax protein interaction with its inhibitor Bcl-xL proteins, without BH3-only proteins. The model has two compartments, the cytosol and the outer mitochondrial membrane. The mechanisms included were translocation of Bax between the compartments, its two-stage activation through incorporation into the membrane and exposure of its BH3 domain, formation of Bax homodimers and its heterodimers with Bcl-xL, the positive feedback from activated Bax. The model exhibits explosive dynamics with saturation when the threshold stimulus is exceeded. The bistability observed in the system belongs to the “trigger” class (the system can return to the lower branch when the stimulus is removed), but exists in a relatively narrow range of parameters. A structural study of the system properties shows that it is the Bax dimerization in heterodimer with Bcl-xL, homodimerization, Bax autoactivation and Bax retrotranslocation that produces a bistable system of the “trigger” type. These results suggest that pair of Bax and Bcl-xL is sufficient for a trigger and the model developed in can be used for studies of relevant intrinsic apoptotic signaling pathways that do not involve BH3-only proteins, such as those initiated by the oxidative stress of the cell.
{"title":"Bistability in the regulatory system of the intrinsic apoptotic pathway arising from the Bax and Bcl-xL interactions","authors":"Ruslan M. Timchenko , Mikhail A. Panteleev","doi":"10.1016/j.jtbi.2025.112344","DOIUrl":"10.1016/j.jtbi.2025.112344","url":null,"abstract":"<div><div>The intrinsic pathway of apoptosis mediates programmed cell death in several major scenarios, but mechanisms regulating its triggering remain unclear. We developed a kinetic mathematical model based on ordinary differential equations and the law of mass action to investigate whether bistability in the regulatory system of the intrinsic apoptotic pathway can be achieved purely on the basis of Bax protein interaction with its inhibitor Bcl-xL proteins, without BH3-only proteins. The model has two compartments, the cytosol and the outer mitochondrial membrane. The mechanisms included were translocation of Bax between the compartments, its two-stage activation through incorporation into the membrane and exposure of its BH3 domain, formation of Bax homodimers and its heterodimers with Bcl-xL, the positive feedback from activated Bax. The model exhibits explosive dynamics with saturation when the threshold stimulus is exceeded. The bistability observed in the system belongs to the “trigger” class (the system can return to the lower branch when the stimulus is removed), but exists in a relatively narrow range of parameters. A structural study of the system properties shows that it is the Bax dimerization in heterodimer with Bcl-xL, homodimerization, Bax autoactivation and Bax retrotranslocation that produces a bistable system of the “trigger” type. These results suggest that pair of Bax and Bcl-xL is sufficient for a trigger and the model developed in can be used for studies of relevant intrinsic apoptotic signaling pathways that do not involve BH3-only proteins, such as those initiated by the oxidative stress of the cell.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"620 ","pages":"Article 112344"},"PeriodicalIF":2.0,"publicationDate":"2025-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145764600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-09DOI: 10.1016/j.jtbi.2025.112330
Anca Rǎdulescu , Richard Halpern , Drew Kozlowski
The study of intra-guild interactions in an ecosystem is an active and impactful direction of inquiry. This is true in particular for fragile systems in which even small perturbations of their functional parameters can produce dramatic effects like species endangerment or extinction, leading the system to enter an unsustainable regime and eventually collapse. In this context, it is important to understand which factors can lead to such effects and for which systems, so that one can act proactively and timely to prevent them. We built and studied a mathematical model that captures the natural interactions in an intra-guild, three species system (i.e., in which two species are predators of the third, but such that one of the predators also consumes the other). The nonlinear components of the model were documented on existing literature and assembled as a system of Lotka-Volterra ordinary differential equations. Our analytical computations and numerical explorations revealed sequences of transcritical and Hopf bifurcations underlying counterintuitive transitions of the system into regions of vulnerability to external noise. We conclude that, in order to avoid extinction, one needs to rigorously prescribe a well-documented, prediction-based approach to population control.
{"title":"A model of predation and survival in a system of three interacting species","authors":"Anca Rǎdulescu , Richard Halpern , Drew Kozlowski","doi":"10.1016/j.jtbi.2025.112330","DOIUrl":"10.1016/j.jtbi.2025.112330","url":null,"abstract":"<div><div>The study of intra-guild interactions in an ecosystem is an active and impactful direction of inquiry. This is true in particular for fragile systems in which even small perturbations of their functional parameters can produce dramatic effects like species endangerment or extinction, leading the system to enter an unsustainable regime and eventually collapse. In this context, it is important to understand which factors can lead to such effects and for which systems, so that one can act proactively and timely to prevent them. We built and studied a mathematical model that captures the natural interactions in an intra-guild, three species system (i.e., in which two species are predators of the third, but such that one of the predators also consumes the other). The nonlinear components of the model were documented on existing literature and assembled as a system of Lotka-Volterra ordinary differential equations. Our analytical computations and numerical explorations revealed sequences of transcritical and Hopf bifurcations underlying counterintuitive transitions of the system into regions of vulnerability to external noise. We conclude that, in order to avoid extinction, one needs to rigorously prescribe a well-documented, prediction-based approach to population control.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"620 ","pages":"Article 112330"},"PeriodicalIF":2.0,"publicationDate":"2025-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145745840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The receptor-binding domain (RBD) of the spike protein is a critical functional component responsible for binding between the SARS-CoV-2 and the ACE2 receptor, as well as monoclonal antibodies. This research focuses on evaluating the ability of SARS-CoV-2 variants to reduce or evade neutralizing antibody responses. The RBD structures of wild type, Delta, and Omicron structures along with nine RBD-directed antibodies downloaded from the Protein Data Bank were subjected to docking simulations via the HADDOCK 2.4 server to calculate Haddock score, binding affinity (ΔG) and dissociation constant (Kd). The resulting complexes underwent molecular dynamics simulations for 100 ns using GROMACS, and the binding free energy was calculated using gmx_MMPBSA. The findings indicated that the L452R and T478K mutations in Delta, as well as the K417N, E484A, S477N, and Q493R mutations in Omicron, were predicted to be pivotal factors in the interaction with antibodies. Omicron exhibited a greater potential for immune evasion compared to Delta. Notably, the Sotrovimab antibody demonstrated robust interactions with both variants. Etesevimab exhibited strong binding with Delta but displayed a weaker connection with Omicron. Therefore, Sotrovimab and Etesevimab remain promising candidates for in vitro and in vivo testing against SARS-CoV-2 variants.
{"title":"Antibody escape of SARS-CoV-2 variants of concern on receptor-binding domain: A computational approach","authors":"Dac-Nhan Nguyen , Quoc-Thai Nguyen , Thoai-My Dang , Phuong-Uyen Tran-Thi , Viet-Hung Tran , Minh-Tri Le , Lam-Truong Tuong , Van-Thanh Tran , Phuong Nguyen Hoai Huynh , Khac-Minh Thai","doi":"10.1016/j.jtbi.2025.112345","DOIUrl":"10.1016/j.jtbi.2025.112345","url":null,"abstract":"<div><div>The receptor-binding domain (RBD) of the spike protein is a critical functional component responsible for binding between the SARS-CoV-2 and the ACE2 receptor, as well as monoclonal antibodies. This research focuses on evaluating the ability of SARS-CoV-2 variants to reduce or evade neutralizing antibody responses. The RBD structures of wild type, Delta, and Omicron structures along with nine RBD-directed antibodies downloaded from the Protein Data Bank were subjected to docking simulations via the HADDOCK 2.4 server to calculate Haddock score, binding affinity (<em>ΔG</em>) and dissociation constant (<em>K<sub>d</sub></em>). The resulting complexes underwent molecular dynamics simulations for 100 ns using GROMACS, and the binding free energy was calculated using gmx_MMPBSA. The findings indicated that the L452R and T478K mutations in Delta, as well as the K417N, E484A, S477N, and Q493R mutations in Omicron, were predicted to be pivotal factors in the interaction with antibodies. Omicron exhibited a greater potential for immune evasion compared to Delta. Notably, the Sotrovimab antibody demonstrated robust interactions with both variants. Etesevimab exhibited strong binding with Delta but displayed a weaker connection with Omicron. Therefore, Sotrovimab and Etesevimab remain promising candidates for <em>in vitro</em> and <em>in vivo</em> testing against SARS-CoV-2 variants.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"619 ","pages":"Article 112345"},"PeriodicalIF":2.0,"publicationDate":"2025-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145710607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-03DOI: 10.1016/j.jtbi.2025.112329
Isobel R. Abell , Thao P. Le , Jennifer A. Flegg , Christopher M. Baker
Varroa destructor is a significant European honeybee pest, impacting agricultural industries globally. Since arriving in 2022, Australia faces the possibility that Varroa will become established in European honeybee colonies nationally. Australia initially pursued a strategy of testing and subsequently eliminating hives infested with Varroa. These management efforts raise interesting questions about the interplay between hive testing and elimination, and the spread of Varroa between hives. This study uses mathematical modelling to investigate how combined hive testing and elimination strategies impact the spread of Varroa through a network of European honeybee hives. We develop a model of both within-hive reproduction of Varroa and hive testing, and between-hive movement of Varroa on a network of hives. This model is used to assess the impact of various testing and hive elimination strategies on the total number of hives eliminated on the network of hives. Each model simulation starts with a single infested hive, and from this we observed one of two dynamics: either the infestation is caught before spreading, or Varroa spreads extensively through the network before being caught by testing. Within our model we implement two common hive testing methods – sugar shake and alcohol testing. A shared limitation of these testing methods is that they can only detect mites in a specific stage of their lifecycle. As such, testing is not only dependent on how many Varroa mites are in a hive, but also on what lifecycle stage the mites are in at the time of testing. By varying testing and movement parameters, we see that this testing limitation greatly impacts the number of hives eliminated in various scenarios. Furthermore, testing earlier, or testing more frequently, does not guarantee a smaller invasion. Our model results suggest irregular testing schedules, e.g. testing multiple times in close succession rather than just once in a given timeframe, may help overcome the limitations of common hive testing strategies.
{"title":"Modelling the spread and management of Varroa destructor in naive european honeybee populations","authors":"Isobel R. Abell , Thao P. Le , Jennifer A. Flegg , Christopher M. Baker","doi":"10.1016/j.jtbi.2025.112329","DOIUrl":"10.1016/j.jtbi.2025.112329","url":null,"abstract":"<div><div><em>Varroa destructor</em> is a significant European honeybee pest, impacting agricultural industries globally. Since arriving in 2022, Australia faces the possibility that <em>Varroa</em> will become established in European honeybee colonies nationally. Australia initially pursued a strategy of testing and subsequently eliminating hives infested with <em>Varroa</em>. These management efforts raise interesting questions about the interplay between hive testing and elimination, and the spread of <em>Varroa</em> between hives. This study uses mathematical modelling to investigate how combined hive testing and elimination strategies impact the spread of <em>Varroa</em> through a network of European honeybee hives. We develop a model of both within-hive reproduction of <em>Varroa</em> and hive testing, and between-hive movement of <em>Varroa</em> on a network of hives. This model is used to assess the impact of various testing and hive elimination strategies on the total number of hives eliminated on the network of hives. Each model simulation starts with a single infested hive, and from this we observed one of two dynamics: either the infestation is caught before spreading, or <em>Varroa</em> spreads extensively through the network before being caught by testing. Within our model we implement two common hive testing methods – sugar shake and alcohol testing. A shared limitation of these testing methods is that they can only detect mites in a specific stage of their lifecycle. As such, testing is not only dependent on how many <em>Varroa</em> mites are in a hive, but also on what lifecycle stage the mites are in at the time of testing. By varying testing and movement parameters, we see that this testing limitation greatly impacts the number of hives eliminated in various scenarios. Furthermore, testing earlier, or testing more frequently, does not guarantee a smaller invasion. Our model results suggest irregular testing schedules, e.g. testing multiple times in close succession rather than just once in a given timeframe, may help overcome the limitations of common hive testing strategies.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"622 ","pages":"Article 112329"},"PeriodicalIF":2.0,"publicationDate":"2025-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145688186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-02DOI: 10.1016/j.jtbi.2025.112331
Juan Segura , Marcos Marvá , Daniel Franco
Habitat fragmentation is a leading cause of biodiversity loss, and efforts to enhance connectivity through, for example, biological corridors are a common conservation strategy to mitigate it. However, understanding the effects of dispersal variation on the total biomass of spatially structured populations is still far from being well understood. For the simplest situation, i.e., a population occupying a habitat divided into two patches, recent studies have shown that there are only four possible response scenarios to increased connectivity in discrete- and continuous-time models under Beverton-Holt and logistic local dynamics, respectively. This paper explores whether the number of patches in a metapopulation influences the number of response scenarios to increased dispersal. We will show that for given local dynamics the number of possible response scenarios significantly increases when the number of patches increases from two to three. Moreover, the paper revisits the problem of how network topology affects total biomass dynamics for low dispersal rates. We will show that the previous claim that bidirectional connectivity always increases biomass at low dispersal rates when connecting sources is false. Indeed, we will prove that transiting from a chain topology to a ring topology can either increase or decrease the total biomass for low dispersal rates if one considers more realistic production functions or if the probability of using a concrete path is not the same in the whole metapopulation.
{"title":"Dispersal in multi-patch metapopulations: The impact of patch number and network topology","authors":"Juan Segura , Marcos Marvá , Daniel Franco","doi":"10.1016/j.jtbi.2025.112331","DOIUrl":"10.1016/j.jtbi.2025.112331","url":null,"abstract":"<div><div>Habitat fragmentation is a leading cause of biodiversity loss, and efforts to enhance connectivity through, for example, biological corridors are a common conservation strategy to mitigate it. However, understanding the effects of dispersal variation on the total biomass of spatially structured populations is still far from being well understood. For the simplest situation, i.e., a population occupying a habitat divided into two patches, recent studies have shown that there are only four possible response scenarios to increased connectivity in discrete- and continuous-time models under Beverton-Holt and logistic local dynamics, respectively. This paper explores whether the number of patches in a metapopulation influences the number of response scenarios to increased dispersal. We will show that for given local dynamics the number of possible response scenarios significantly increases when the number of patches increases from two to three. Moreover, the paper revisits the problem of how network topology affects total biomass dynamics for low dispersal rates. We will show that the previous claim that bidirectional connectivity always increases biomass at low dispersal rates when connecting sources is false. Indeed, we will prove that transiting from a chain topology to a ring topology can either increase or decrease the total biomass for low dispersal rates if one considers more realistic production functions or if the probability of using a concrete path is not the same in the whole metapopulation.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"619 ","pages":"Article 112331"},"PeriodicalIF":2.0,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145679323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-29DOI: 10.1016/j.jtbi.2025.112332
Yusuke Ikegawa , Chihiro Himuro , Atsushi Honma
Reproductive interference (RI) includes any negative effect on reproductive success of females that is induced by interspecific sexual interactions. Although previous population dynamic models of RI have focused on population-level processes (e.g., changes in population size), individual-level processes (e.g., search and courtship by males and subsequent choice by females) have been largely overlooked. In this study, we constructed a discrete-time population dynamic model comprising two species, assuming iterative courtship and mating within each reproductive time period (i.e., individual-level process) and subsequent population dynamics (i.e., population-level process). We assumed that if males (or females) have wide acceptance range to their counterparts, correct courtship (or mating) to conspecifics and incorrect courtship to heterospecifics would increase simultaneously. We also assumed that two species have different demographics (species 1 with higher reproduction and mortality, species 2 with lower reproduction and mortality). We showed that intermediate acceptance range of females mitigated the negative effect of courtship from heterospecific males on mating success. However, the initially more abundant species 1 can be outcompeted by the initially less abundant species 2. This is because the net negative effect of losing mating opportunities due to RI was greater for species 1 with higher mortality than for species 2 with lower mortality. Overall, the results of reproductive success, which are derived only from individual-level processes, are not always consistent with the demographic consequences, which are derived from both individual- and population-level processes. We propose that analyzing the RI system by considering both individual- and population-level processes is necessary.
{"title":"Demographic consequences of the loss of mating opportunities in a two-species reproductive interference system","authors":"Yusuke Ikegawa , Chihiro Himuro , Atsushi Honma","doi":"10.1016/j.jtbi.2025.112332","DOIUrl":"10.1016/j.jtbi.2025.112332","url":null,"abstract":"<div><div>Reproductive interference (RI) includes any negative effect on reproductive success of females that is induced by interspecific sexual interactions. Although previous population dynamic models of RI have focused on population-level processes (e.g., changes in population size), individual-level processes (e.g., search and courtship by males and subsequent choice by females) have been largely overlooked. In this study, we constructed a discrete-time population dynamic model comprising two species, assuming iterative courtship and mating within each reproductive time period (i.e., individual-level process) and subsequent population dynamics (i.e., population-level process). We assumed that if males (or females) have wide acceptance range to their counterparts, correct courtship (or mating) to conspecifics and incorrect courtship to heterospecifics would increase simultaneously. We also assumed that two species have different demographics (species 1 with higher reproduction and mortality, species 2 with lower reproduction and mortality). We showed that intermediate acceptance range of females mitigated the negative effect of courtship from heterospecific males on mating success. However, the initially more abundant species 1 can be outcompeted by the initially less abundant species 2. This is because the net negative effect of losing mating opportunities due to RI was greater for species 1 with higher mortality than for species 2 with lower mortality. Overall, the results of reproductive success, which are derived only from individual-level processes, are not always consistent with the demographic consequences, which are derived from both individual- and population-level processes. We propose that analyzing the RI system by considering both individual- and population-level processes is necessary.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"619 ","pages":"Article 112332"},"PeriodicalIF":2.0,"publicationDate":"2025-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145650219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-29DOI: 10.1016/j.jtbi.2025.112317
Griffin Kutler Dodd, Rob J. de Boer
The current standard treatment for HIV-1 infection is antiretroviral therapy, which effectively suppresses viral replication but requires a lifelong drug regimen. An alternative treatment approach is a single injection of a modified version of the HIV-1 virus, termed a therapeutic interfering particle (TIP), that lacks replication machinery and suppresses the wild-type virus by competing for viral proteins. Here, we derive a novel ordinary differential equation model of TIP dynamics. We confirm results from previous models that TIPs can reduce viral load when doubly infected cells produce at least as many virus particles as singly infected cells. By deriving the basic reproduction number of a TIP, we predict that concurrent antiretroviral therapy should make it more difficult for a TIP to persist in a host. Adding an immune response to our model reveals that even a moderate immune response against virally infected cells drastically decreases the range of parameter values for which therapy is effective. Together, these results show that the success of TIPs depend on the properties of the wild-type virus and even more strongly on the immune response, which makes it hard to predict therapeutic success.
{"title":"Immune responses may make HIV-1 therapeutic interfering particles less effective","authors":"Griffin Kutler Dodd, Rob J. de Boer","doi":"10.1016/j.jtbi.2025.112317","DOIUrl":"10.1016/j.jtbi.2025.112317","url":null,"abstract":"<div><div>The current standard treatment for HIV-1 infection is antiretroviral therapy, which effectively suppresses viral replication but requires a lifelong drug regimen. An alternative treatment approach is a single injection of a modified version of the HIV-1 virus, termed a therapeutic interfering particle (TIP), that lacks replication machinery and suppresses the wild-type virus by competing for viral proteins. Here, we derive a novel ordinary differential equation model of TIP dynamics. We confirm results from previous models that TIPs can reduce viral load when doubly infected cells produce at least as many virus particles as singly infected cells. By deriving the basic reproduction number <span><math><msubsup><mi>R</mi><mn>0</mn><mi>T</mi></msubsup></math></span> of a TIP, we predict that concurrent antiretroviral therapy should make it more difficult for a TIP to persist in a host. Adding an immune response to our model reveals that even a moderate immune response against virally infected cells drastically decreases the range of parameter values for which therapy is effective. Together, these results show that the success of TIPs depend on the properties of the wild-type virus and even more strongly on the immune response, which makes it hard to predict therapeutic success.</div></div>","PeriodicalId":54763,"journal":{"name":"Journal of Theoretical Biology","volume":"619 ","pages":"Article 112317"},"PeriodicalIF":2.0,"publicationDate":"2025-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145649812","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"数学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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