生物学最新文献

This study examines competition models based on the Lotka-Volterra form that incorporate starvation-driven diffusions (SDD). Such dispersal assumes that species disperse in response to resource abundance or scarcity in a heterogeneous habitat. The primary objective of this study is to examine how SDD, in combination with diverse interspecific interactions, affects species' fitness and coexistence states. To this end, the study introduces a refined classification for competing interactions based on a novel metric that quantifies the variability of resource heterogeneity across the environment. This approach contrasts with traditional models that assume uniform diffusion within homogeneous environments. This study investigates the local stability of two semitrivial steady states and establishes the existence and uniqueness of positive steady states by eigenvalue analysis and monotone dynamical systems theory. Through this analytical exploration, the study reveals that the interplay between species' dispersal strategies and the varying intensities of interspecific competition significantly impacts ecological outcomes.

This work examines the dynamics of a discrete-time plankton interaction model, in which phytoplankton generate toxins and are vulnerable to external contamination. The model includes a Holling Type-II predation response and uses a piecewise constant argument approach to break it up into smaller pieces. This keeps the ecological realism of the continuous system while making it possible to study complex discrete-time behaviors. Our focus is on the formation of Neimark-Sacker bifurcation, a phenomena associated with the initiation of quasi-periodic oscillations in population densities. We show how toxin buildup and outside contamination can make plankton populations unstable, which could cause blooms to happen in an irregular way, using stability analysis and numerical simulations. The results show how useful discrete-time models are for capturing rapid changes in ecosystems, such damaging algal blooms. They also give ideas for managing ecosystems and reducing blooms.

COVID-19 infection exhibits significant age-related differences. In this paper, we consider an infectious disease model with age-structure in susceptibility and evolutionary game and analyze the impact of mandatory and voluntary vaccination strategies on disease progression. We derive the conditions for the existence of equilibria and confirm that the basic reproduction number $R_0$ serves as a threshold parameter that fully determines the dynamical properties of the model. Theoretical analyses indicate that the persistence of COVID-19 is contingent upon the value of the basic reproduction number. By conducting numerical simulations, we investigate the impacts of various factors, including relative vaccine cost and vaccine effectiveness, on disease dynamics under a voluntary vaccination policy. Our analysis reveals that enhancing vaccine effectiveness does not reduce disease transmission when vaccination rates are extremely low. Under voluntary vaccination policies, it is crucial to keep relative vaccine costs below a certain threshold to promote higher vaccination uptake.

Based on the considerations of round-trip in the treatment process, this paper presents a mathematical model aimed at studying the dynamic behaviour and epidemiological trends of HIV/AIDS. We first calculate the basic reproduction number ${\bar{R}}_0$ and discuss the stability of equilibrium points and the existence of forward bifurcations, validating the theoretical results through numerical simulations. Subsequently, using cumulative HIV/AIDS case data reported in China, we estimate model parameters using the least squares method, achieving a good fit. Furthermore, sensitivity analyses were performed on the model parameters to explain the dependence of the parameters on the infection variables. Finally, the model is applied to evaluate the control effects of treatment coverage at different stages of infection. The results suggest that reducing HIV/AIDS exposure, improving HIV/AIDS screening, promoting infectious disease treatment and increasing disease prevention awareness are the most effective measures to prevent HIV/AIDS infection.

We extend the predator-prey model developed by Ackleh et al. [Persistence and stability analysis of discrete-time predator-prey models: A study of population and evolutionary dynamics. J. Differ. Equ. Appl. 2019;25:1568-1603] to incorporate the evolution of a predator's resistance to toxicant effects. We consider three cases: (1) lethal effects, where the toxicant directly influences the predator's survival; (2) sublethal effects, where the toxicant impacts the predator's fecundity, and (3) mixed effects, where the toxicant impacts both vital rates. For the first two cases, we derive conditions for existence and stability of model equilibria and for system persistence. These cases are also analyzed numerically to further understand the system dynamics. Overall, we find that evolution of a predator to resist a toxicant may allow for predator survival when otherwise it would have faced extinction. However, evolution in response to lethal effects can generate multiple boundary equilibria, leading to alternative stable states. When this occurs, evolution in response to a toxicant may result in the extinction of the predator while, without evolution, the predator survives.

Severe fever with thrombocytopenia syndrome (SFTS), caused by Dabie bandavirus (SFTS virus, SFTSV), poses a growing public health concern in East Asia. Limited genomic data from Shandong Province have restricted understanding of viral evolution, while codon usage bias, a key factor in viral fitness and host adaptation, remains uncharacterized. In this study, we analyzed codon usage patterns in SFTSV strains from Shandong using newly 152 sequenced samples and publicly available genomes. Phylogenetic analysis identified seven genotypes, with genotype A being dominant. Viral genomes showed higher adenine (A) and guanine (G) content and a tendency to use G or cytosine (C) at the third codon position. Relative synonymous codon usage analysis demonstrated gene-specific preferences for codons ending in G/C. Effective number of codons values indicated weak overall codon usage bias. Further analyses suggested that both mutation pressure and natural selection influence codon usage, with natural selection playing the dominant role (52.8-91.4%), particularly in the nucleoprotein (91.4%) and nonstructural genes (89.5%). Codon adaptation index analysis across 12 host species indicated stronger codon adaptation to humans and Gallus gallus, implying higher viral replication efficiency in these hosts. Overall, codon usage bias is primarily driven by natural selection rather than mutation pressure. These findings improve understanding of SFTSV molecular evolution and may inform strategies for surveillance, vaccine design, and host-specific intervention.

Actinobacillus pleuropneumoniae causes porcine infectious pleuropneumonia in pigs. We aimed to characterize the phenotypic and genomic features of three A. pleuropneumoniae strains from clinical cases in eastern Chinese provinces. The serovar 5 strain ZJNH2023 was more pathogenic than strains AH2020 and ZJXS2022 in a murine model and was resistant to multiple antimicrobials. The core genome SNP (single nucleotide polymorphism) tree indicates that the three isolates are clustered with serovars 5, 8, and 15 strains of archived genomes. They harbor plasmids conferring resistance to florfenicol and are of substantial genome diversity, having more prophages, genomic islands (GIs), and antimicrobial resistance genes (ARGs) than the strains of corresponding serovars from other studies. The capsule-related gene clusters in strains AH2022 and ZJXS2022 are different from ZJNH2023 and contain an ISApl1 family transposase between the cps and cpx loci. The serovar 5 strain ZJNH2023 has a full set of ApxI genes, Apa1/Apa2, intact flp family genes related to Flp pilus assembly, and a full set tadABCD genes related to adherence, while strains ZJXS2022 and AH2022 carry ApxIII gene set, lack ApxIAC genes and Apa1/Apa2, and do not have intact flp family genes. Thus, we conclude that possession of the cytotoxic ApxI gene set and those involved in adhesion contributes to higher pathogenicity of the serovar 5 strain ZJNH2023. Distinct GIs and floR-containing plasmids in these strains might have been involved in multiple resistance and horizontal transfer of ARGs on the pig farms.

In this paper, we introduce a mathematical simulation that captures the dynamics of lumpy skin disease (LSD) by considering three key transmission paths: vector-borne, direct cattle-to-cattle contact and environmental contamination. Additionally, this model incorporates three control measures, including vector control, environmental management and isolation/treatment of infected cattle. We perform a comprehensive mathematical analysis to demonstrate the model well-posedness, like proving the existence, uniqueness, positivity and boundedness of the solution. The basic reproduction number ($R_0$) is calculated. The local and global stability analysis is presented for the disease-free and endemic equilibrium points. Sensitivity analysis for the model parameters is shown, which reveals that isolation and treatment control measures are the most effective in eliminating disease transmission. We construct an objective function to formulate an optimal control problem (OCP) and derive the optimality necessary conditions. Numerical simulations confirm the theoretical findings, demonstrating that strategic implementation of combined control measures can efficiently suppress LSD.

Human T-lymphotropic virus (HTLV) and human immunodeficiency virus (HIV) are two retroviruses that pose a certain threat to human psychology and physiology. In this paper, we propose a diffusive HTLV and HIV coinfection model with macrophages, two delays, cell-to-cell transmission and three latently infected cells in which latent HIV infected CD4${}^{+}$T cells, latent HIV infected macrophages, and latent HTLV infected CD4${}^{+}$T cells are considered. Four reproduction number and four equilibria, namely, infection-free equilibrium, HIV infection equilibrium, HTLV infection equilibrium and HTLV and HIV coinfection equilibrium, are calculated and proved the global asymptotic stability of the coinfection model. Numerical simulations are executed to showcase the corresponding theoretical outcomes and uncover how macrophages and latently infected cells influence the dynamics of HTLV and HIV coinfection.

Swine viral infections continue to impose major economic and animal-health burdens worldwide, with pathogens such as porcine epidemic diarrhea virus (PEDV), African swine fever virus (ASFV), and porcine reproductive and respiratory syndrome virus (PRRSV) causing recurrent outbreaks. Autophagy and ubiquitination are central degradative pathways that act as double-edged swords, serving both host defense and viral exploitation. In this narrative review, we synthesize recent advances showing how these pathogens manipulate ubiquitin - autophagy circuits while host cells counteract through selective autophagy. We propose an autophagy - metabolism - immunity triad that positions autophagy as a hub linking infection, metabolic reprogramming, and immune evasion. This integrated framework moves beyond the traditional view of autophagy as strictly antiviral or pro-viral. Deciphering how viruses hijack ubiquitin - autophagy axes reveals actionable therapeutic targets and translational opportunities for antivirals, adjuvants, and metabolic interventions to reduce the burden of swine viral diseases.