{"title":"Fractional gender structured model of human papillomavirus (HPV).","authors":"Veysel Fuat Hatipoğlu, Maia Martcheva","doi":"10.3934/mbe.2026062","DOIUrl":"10.3934/mbe.2026062","url":null,"abstract":"<p><p>We propose a fractional-order differential equation model to study the gender-specific transmission dynamics of human papillomavirus (HPV). Due to limited gender-disaggregated HPV data, oropharyngeal cancer incidence was used as a proxy. The model includes a theoretical analysis of disease-free and endemic equilibria and computation of the basic reproduction number, with stability conditions derived for both cases. Structural identifiability was confirmed using differential algebra, and data fitting indicated that the fractional models $ (alpha = 0.9) $ better captured U.S. dynamics, while classical models $ (alpha = 1) $ suited Turkish data. Practical identifiability, assessed via Monte Carlo simulations, revealed that most parameters were identifiable, though some (e.g., the male exit rate $ mu_m $) showed limitations. Numerical simulations demonstrated sensitivity to fractional effects. This work provides a robust framework for modeling the transmission of HPV and offers insights for future epidemiological modeling and intervention planning.</p>","PeriodicalId":49870,"journal":{"name":"Mathematical Biosciences and Engineering","volume":"23 6","pages":"1708-1742"},"PeriodicalIF":2.6,"publicationDate":"2026-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148450254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Exploring the effect of density dependent infection rate in a within host viral infection model.","authors":"Hope Sage, Hana M Dobrovolny","doi":"10.3934/mbe.2026061","DOIUrl":"https://doi.org/10.3934/mbe.2026061","url":null,"abstract":"<p><p>The most common viral dynamics models for analyzing viral infections assume a well-mixed spatial distribution between viral particles and uninfected target cells. However, throughout an infection, the spatial distribution of virus and cells changes. Initially, virus and infected cells are localized so that a target cell in an area with lower virus presence will be less likely to be infected than a cell close to a location of viral production. A density-dependent infection rate has the potential to improve models that treat the cellular infection probability as a constant. Building on previous work that used epidemiological models, which introduced Saturated Incidence, Beddington-DeAngelis, and Crowley Martin models to simulate spatial heterogeneity in population-level models, we implemented these density-dependent models in within-host viral kinetics models to understand how a density dependent infection rate might impact the predicted severity of an influenza infection. The parameter values that govern the strength of density dependence were varied to understand the implications of density dependent infection rate on disease severity and the potential impacts on patient treatment. For low density dependence, a steeper increase in the virus and a higher viral peak was predicted. We find that the initial localization of infected cells slows the progression of the infection, thus suggesting that accounting for density dependence when analyzing influenza infection severity can result in an altered expectation for viral progression.</p>","PeriodicalId":49870,"journal":{"name":"Mathematical Biosciences and Engineering","volume":"23 6","pages":"1687-1707"},"PeriodicalIF":2.6,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148450324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mackenzie Dalton, Emmanuel Asante-Asamani, James Greene
{"title":"A simple mechanistic model for insulin-glucose-glucagon dynamics and its implications for diabetes management.","authors":"Mackenzie Dalton, Emmanuel Asante-Asamani, James Greene","doi":"10.3934/mbe.2026060","DOIUrl":"https://doi.org/10.3934/mbe.2026060","url":null,"abstract":"<p><p>Insulin and glucose dynamics are tightly regulated by the pancreatic islets of Langerhans, which contain beta cells that produce insulin and alpha cells that produce glucagon. Insulin lowers blood glucose by enabling cells to access glucose for energy, while glucagon raises blood glucose levels by stimulating the liver to produce glucose from non-carbohydrate sources as well as breaking down stored glycogen. Maintaining safe blood glucose levels is crucial, as both high (hyperglycemia) and low (hypoglycemia) levels can lead to life threatening consequences. In this work, a simple three-state mechanistic insulin-glucose-glucagon model is developed and validated using data from pigs subjected to an intravenous glucose tolerance test (IVGTT). The model is then used to investigate glucose and glucagon dynamics in patients administering exogenous insulin, shedding light on the impact of improper diabetes management. The results show that delayed administration of exogenous insulin increases the risk of hypoglycemia by suppressing glucagon production. Furthermore, insulin half-lives of 60 minutes or longer were tested, revealing that such prolonged exogenous insulin activity can suppress glucagon's response to critically low glucose levels. This finding suggests that shorter insulin half-lives may help reduce the risk of hypoglycemic events.</p>","PeriodicalId":49870,"journal":{"name":"Mathematical Biosciences and Engineering","volume":"23 6","pages":"1651-1686"},"PeriodicalIF":2.6,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148450182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A nonlinear time-delay modeling case study of Tuberculosis transmission in Algeria: 1990-2024.","authors":"Nadjla Abidat, Akhil Kumar Srivastav, Nico Stollenwerk, Abderrazak NABTi, Maíra Aguiar","doi":"10.3934/mbe.2026059","DOIUrl":"https://doi.org/10.3934/mbe.2026059","url":null,"abstract":"<p><p>This study develops a nonlinear time-delay mathematical model to investigate the transmission dynamics of tuberculosis in Algeria over the period 1990-2024. The model explicitly incorporates a delay representing the incubation period between infection and the onset of infectiousness, which significantly affects system behavior by potentially inducing instability and oscillatory dynamics. In particular, increasing the delay can destabilize the endemic equilibrium and lead to periodic outbreaks through Hopf bifurcation. The basic reproduction number $ mathcal{R}_0 $ is derived, and rigorous analysis establishes the local and global stability conditions for both disease-free and endemic equilibria. Sensitivity analysis identifies key epidemiological parameters influencing $ mathcal{R}_0 $, providing insight into effective intervention strategies. From a public health perspective, the results highlight that reducing diagnostic delays and improving timely treatment can stabilize disease dynamics and prevent recurrent outbreaks. Numerical simulations, calibrated with Algerian tuberculosis data from 1990 to 2024, support the theoretical findings and demonstrate the critical role of delay effects in shaping tuberculosis transmission and control.</p>","PeriodicalId":49870,"journal":{"name":"Mathematical Biosciences and Engineering","volume":"23 6","pages":"1622-1650"},"PeriodicalIF":2.6,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148450143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Stabilizing predator-prey interactions: the impact of supplementary food and anti-predator behavior.","authors":"Aladeen Al Basheer","doi":"10.3934/mbe.2026058","DOIUrl":"https://doi.org/10.3934/mbe.2026058","url":null,"abstract":"<p><p>This study investigated a modified Holling-Tanner predator-prey model that incorporates supplementary food for predators and anti-predator behavior in prey. The model examined how these ecological mechanisms influence predator-prey dynamics and biological pest control. Local and global stability analyses were performed to determine the conditions that lead to predator persistence and pest eradication. Explicit parametric conditions were derived that guarantee global pest extinction, providing quantitative criteria for effective biological control. Bifurcation analysis revealed the presence of Hopf and saddle-node bifurcations, which identify critical parameter thresholds where the system transitions between stable equilibria, oscillatory dynamics, and collapse of coexistence states. The results showed that anti-predator behavior can stabilize population dynamics and suppress oscillatory behavior that would otherwise occur in the absence of prey defense mechanisms. A reaction-diffusion extension of the model was then considered to investigate spatial effects. Turing instability analysis demonstrated that the interaction between diffusion and anti-predator behavior can generate persistent spatial patterns, offering a mechanistic explanation for patchy predator distributions frequently observed in agricultural ecosystems. The analysis further indicated that the effectiveness of biological control depends on the balance between supplementary food quantity, predation pressure, and the strength of prey defense. Excessive food supplementation may reduce predator pressure on pests and weaken pest suppression. Numerical simulations supported the analytical results and illustrated parameter regimes that lead to system stabilization and successful pest management. The proposed framework provides theoretical guidance for designing predator-based biological control strategies that combine resource provisioning with natural behavioral responses.</p>","PeriodicalId":49870,"journal":{"name":"Mathematical Biosciences and Engineering","volume":"23 6","pages":"1593-1621"},"PeriodicalIF":2.6,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148450299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effects of a protection zone in a reaction-advection-diffusion model with strong Allee effect.","authors":"Davis Henderson, Bingtuan Li","doi":"10.3934/mbe.2026057","DOIUrl":"https://doi.org/10.3934/mbe.2026057","url":null,"abstract":"<p><p>We consider a reaction-advection-diffusion equation that models a population in a bounded habitat with a strong Allee effect and a protection zone. We assume that the population growth function exhibits the strong Allee effect and has a positive integral within the protection zone (indicating population persistence) and a negative integral in the surrounding patches (indicating population decay). We prove that the existence of positive steady-state solutions to this system depends on the length of the protection zone. It is demonstrated that there exists a threshold value $ H^* $ such that, for a protection zone of size $ H^* $, there exists one positive steady-state solution and, for a larger protection zone, there exist multiple positive steady-state solutions. For smaller protection zones, we prove there exists no positive steady-state solution. The dynamics of the equation are further examined via numerical simulations.</p>","PeriodicalId":49870,"journal":{"name":"Mathematical Biosciences and Engineering","volume":"23 6","pages":"1572-1592"},"PeriodicalIF":2.6,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148450196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Taurai Mademutsa, Mark Kimathi, Jeconia Okello Abonyo, Tinashe Byron Gashirai
{"title":"A multi-strain sequential super-infection model for dengue fever with antibody dependent enhancement.","authors":"Taurai Mademutsa, Mark Kimathi, Jeconia Okello Abonyo, Tinashe Byron Gashirai","doi":"10.3934/mbe.2026056","DOIUrl":"https://doi.org/10.3934/mbe.2026056","url":null,"abstract":"<p><p>Dengue fever is a vector-borne disease that is transmitted by the <i>aedes aegypti</i> mosquito. The disease is caused by four different viral serotypes which are DEN-1, DEN-2, DEN-3, and DEN-4. Of these serotypes, DEN-1 and DEN-2 are the most prevalent, and their co-circulation presents complex disease dynamics due to the antibody-dependent enhancement (ADE) phenomenon as well as the cross-immunity interaction of these viral serotypes. In this study, we formulate a novel multi-strain sequential super-infection model that captures the primary and secondary infection dynamics with temporary cross immunity, asymptomatic infections, and enhancement in disease transmissibility due to antibody-dependent enhancement (ADE) upon heterologous reinfection. Our analyses revealed that significant secondary infections cause a backward bifurcation phenomena due to changes in the biting rate $ b $, which maintains disease endemicity when the basic reproduction number is below unity. The implications of this phenomena are that intervention measures would need to target a critical threshold of $ mathcal{R}_{0} $ associated with $ b_c $, below which we are assured of disease elimination. Numerical analysis showed that the values of $ b_{c} $ are highly influenced by changes in the ADE. Thus effective control of dengue fever requires intensified and sustained control methods that drive transmission below critical thresholds. The findings of this study shed light on critical insights in the design and implementation of eradication measures in dengue fever endemic regions.</p>","PeriodicalId":49870,"journal":{"name":"Mathematical Biosciences and Engineering","volume":"23 6","pages":"1534-1571"},"PeriodicalIF":2.6,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148450213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Marius Tadjuidje Fodjo, Aurelien Kambeu Youmbi, Maison Mayeh, Solange Whegang, Bruno Kenfack, Berge Tsanou
{"title":"Modeling the impact of budget limitation on the screening and treatment pathway of HPV-induced precancerous cervical lesions.","authors":"Marius Tadjuidje Fodjo, Aurelien Kambeu Youmbi, Maison Mayeh, Solange Whegang, Bruno Kenfack, Berge Tsanou","doi":"10.3934/mbe.2026055","DOIUrl":"10.3934/mbe.2026055","url":null,"abstract":"<p><p>Cervical cancer in women remains a major public health challenge in sub-Saharan Africa, where both the late diagnoses and limited financial resources hinder effective prevention and treatment. We propose an economic-epidemiological model that integrates the care pathway for cervical lesions and the financial ability to access different treatment stages. Analytical results establish the existence of a basic economic threshold $ mathcal{R}_0 $, whose value determines whether the system sustains preventive care or collapses into diagnostic failure. We show that a backward bifurcation can occur when $ mathcal{R}_0 < 1 $, leading to the coexistence of two stable equilibrium points. Furthermore, we establish the global stability of the system collapse equilibrium when $ mathcal{R}_0 leq 1 $ under specific conditions. Sensitivity analysis identifies key economic parameters such as screening subsidy, treatment cost, and patient contribution to the billing account that critically influence model dynamics. Numerical simulations estimate that a minimum subsidy level of approximately 13.1% of the human papillomavirus (HPV) test cost is required to ensure system viability ($ mathcal{R}_0 > 1 $) and prevent long-term collapse of screening coverage. We further decompose the total treatment cost across the care stages and formulate an optimization problem to determine the optimal allocation of government subsidies, minimizing treatment costs while ensuring 90% coverage of women who test positive for HPV. The results show that the optimal strategy requires the government to cover 21.65% of the total treatment cost, mainly focusing on the eligibility test and Large loop excision of the transformation zone (LLETZ) treatment. These findings highlight the importance of targeted subsidies to guarantee both accessibility and financial sustainability in the treatment of precancerous cervical lesions.</p>","PeriodicalId":49870,"journal":{"name":"Mathematical Biosciences and Engineering","volume":"23 5","pages":"1501-1533"},"PeriodicalIF":2.6,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147943492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ananta Acharya, Emily Cosgrove, James T Cronin, Jerome Goddard Ⅱ, Eddie Lindsey, Amila Muthunayake, Dustin Nichols, Ratnasingham Shivaji
{"title":"Modeling the effects of trait-mediated dispersal on coexistence of two species: Competition and non-consumptive predator-prey.","authors":"Ananta Acharya, Emily Cosgrove, James T Cronin, Jerome Goddard Ⅱ, Eddie Lindsey, Amila Muthunayake, Dustin Nichols, Ratnasingham Shivaji","doi":"10.3934/mbe.2026054","DOIUrl":"10.3934/mbe.2026054","url":null,"abstract":"<p><p>Fragmentation and loss of habitat owing to increased human activity are major drivers of species extinctions and declining global biodiversity. In ecological communities, trait-mediated indirect effects are frequently observed and can influence population dynamics as strongly, possibly even more strongly, than direct effects. However, few studies have focused on trait-mediated behavior such as trait-mediated dispersal, in which the dispersal patterns are altered by the presence of an interacting species. Moreover, little is known about how trait-mediated dispersal interacts with habitat fragmentation and loss to affect the coexistence of interacting species. Here, we explore the consequences of both trait-mediated dispersal and fragmentation/loss on coexistence in a system consisting of two competing species or a predator and its prey. By assuming that the density-mediated effects are negligible, we isolate the role of trait-mediated effects. Our results show that the combined influence of fragmentation and trait-mediated dispersal can substantially reshape the population dynamics and species coexistence outcomes.</p>","PeriodicalId":49870,"journal":{"name":"Mathematical Biosciences and Engineering","volume":"23 5","pages":"1461-1500"},"PeriodicalIF":2.6,"publicationDate":"2026-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147943470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A stochastic agent-based model for simulating tumor-immune dynamics and evaluating therapeutic strategies.","authors":"Yuhong Zhang, Chenghang Li, Boya Wang, Jinzhi Lei","doi":"10.3934/mbe.2026052","DOIUrl":"10.3934/mbe.2026052","url":null,"abstract":"<p><p>Tumor-immune interactions are central to understanding cancer progression and treatment outcomes. In this study, we present a stochastic agent-based model that integrates cellular heterogeneity, spatial cell-cell interactions, and the evolution of drug resistance to simulate tumor growth and the immune response in a two-dimensional microenvironment. This model captures the dynamic behaviors of four major cell types, specifically tumor cells, cytotoxic T lymphocytes, helper T cells, and regulatory T cells, and incorporates key biological processes, including proliferation, apoptosis, migration, and immune regulation. Using this framework, we simulate tumor progression under different therapeutic interventions, including radiotherapy, targeted therapy, and immune checkpoint blockade. Our simulations reproduce emergent phenomena such as immune privilege and spatial immune exclusion. Quantitative analyses demonstrate that all therapies suppress tumor growth to varying degrees and reshape the tumor microenvironment. Notably, combination therapies, particularly targeted therapy with immunotherapy, achieve the most effective tumor control. Crucially, sensitivity analyses reveal a distinct hierarchy among therapeutic determinants: Short-term efficacy is predominantly governed by intrinsic drug sensitivity thresholds rather than drug resistance update rates. Furthermore, we identify a response saturation effect that is specific to immunotherapy, where efficacy plateaus beyond a certain sensitivity threshold due to the spatial limits of immune infiltration. This work demonstrates the utility of agent-based models in capturing complex tumor-immune dynamics and provides a computational platform for optimizing cancer treatment strategies. The model is extensible, biologically interpretable, and well-suited for future integration with experimental or clinical data.</p>","PeriodicalId":49870,"journal":{"name":"Mathematical Biosciences and Engineering","volume":"23 5","pages":"1402-1436"},"PeriodicalIF":2.6,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147942801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"工程技术","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}