Search

In this paper, we introduce and analyze a mathematical model of a viral infection with explicit age-since infection structure for infected cells. We extend previous age-structured within-host virus models by including logistic growth of target cells and allowing for absorption of multiple virus particles by infected cells. The persistence of the virus is shown to depend on the basic reproduction number R0. In particular, when R0 ⩽ 1, the infection free equilibrium is globally asymptotically stable, and conversely if R0 > 1, then the infection free equilibrium is unstable, the system is uniformly persistent and there exists a unique positive equilibrium. We show that our system undergoes a Hopf bifurcation through which the infection equilibrium loses the stability and periodic solutions appear. [ABSTRACT FROM AUTHOR]

Mathematical modeling and analysis can provide insight on the dynamics of ecosystems which maintain biodiversity in the face of competitive and prey-predator interactions. Of primary interests are the underlying structure and features which stabilize diverse ecological networks. Recently Korytowski and Smith (Theor Ecol 8(1):111-120, 2015) proved that a perfectly nested infection network, along with appropriate life history trade-offs, leads to coexistence and persistence of bacteria-phage communities in a chemostat model. In this article, we generalize their model in order to apply it to the within-host dynamics virus and immune response, in particular HIV and CTL (Cytotoxic T Lymphocyte) cells. Our model can describe sequential viral escape from dominant immune responses and rise in subdominant immune responses, consistent with observed patterns of HIV/CTL evolution. We find a Lyapunov function for the system which leads to rigorous characterization of persistent viral and immune variants, along with informing upon equilibria stability and global dynamics. Results are interpreted in the context of within-host HIV/CTL evolution and numerical simulations are provided. [ABSTRACT FROM AUTHOR]

The aim of this article is to provide formulas and properties of the basic reproduction number, R0, for a within-host virus model with periodic combination drug treatment. In particular, we extend and further results about how the phase difference between drug treatment can critically affect the asymptotic dynamics of model and corresponding R0. Our main theorem establishes that R0 is minimized for out-of-phase efficacies and maximized for in-phase efficacies in a special case where drug efficacies are\bang-bang" functions. [ABSTRACT FROM AUTHOR]

Contact tracing is an important control strategy for containing Ebola epidemics. From a modeling perspective, explicitly incorporating contact tracing with disease dynamics presents challenges, and population level effects of contact tracing are difficult to determine. In this work, we formulate and analyze a mechanistic SEIR type outbreak model which considers the key features of contact tracing, and we characterize the impact of contact tracing on the effective reproduction number, R e , of Ebola. In particular, we determine how relevant epidemiological properties such as incubation period, infectious period and case reporting, along with varying monitoring protocols, affect the efficacy of contact tracing. In the special cases of either perfect monitoring of traced cases or perfect reporting of all cases, we derive simple formulae for the critical proportion of contacts that need to be traced in order to bring the effective reproduction number R e below one. Also, in either case, we show that R e can be expressed completely in terms of observable reported case/tracing quantities , namely R e = k ( ( 1 − q ) / q ) + k m where k is the number of secondary traced infected contacts per primary untraced reported case, k m is the number of secondary traced infected contacts per primary traced reported case and ( 1 − q ) / q is the odds that a reported case is not a traced contact. These formulae quantify contact tracing as both an intervention strategy that impacts disease spread and a probe into the current epidemic status at the population level. Data from the West Africa Ebola outbreak is utilized to form real-time estimates of R e , and inform our projections of the impact of contact tracing, and other control measures, on the epidemic trajectory. [ABSTRACT FROM AUTHOR]

Mass-vaccination campaigns are an important strategy in the global fight against poliomyelitis and measles. The large-scale logistics required for these mass immunisation campaigns magnifies the need for research into the effectiveness and optimal deployment of pulse vaccination. In order to better understand this control strategy, we propose a mathematical model accounting for the disease dynamics in connected regions, incorporating seasonality, environmental reservoirs and independent periodic pulse vaccination schedules in each region. The effective reproduction number, $$R_e$$ , is defined and proved to be a global threshold for persistence of the disease. Analytical and numerical calculations show the importance of synchronising the pulse vaccinations in connected regions and the timing of the pulses with respect to the pathogen circulation seasonality. Our results indicate that it may be crucial for mass-vaccination programs, such as national immunisation days, to be synchronised across different regions. In addition, simulations show that a migration imbalance can increase $$R_e$$ and alter how pulse vaccination should be optimally distributed among the patches, similar to results found with constant-rate vaccination. Furthermore, contrary to the case of constant-rate vaccination, the fraction of environmental transmission affects the value of $$R_e$$ when pulse vaccination is present. [ABSTRACT FROM AUTHOR]

A mathematical model of a within-host viral infection with explicit age-since-infection structure for infected cells is presented. A global analysis of the model is conducted. It is shown that when the basic reproductive number falls below unity, the infection dies out. On the contrary, when the basic reproductive number exceeds unity, there exists a unique positive equilibrium that attracts all positive solutions of the model. The global stability analysis combines the existence of a compact global attractor and a Lyapunov function. [ABSTRACT FROM AUTHOR]

Floquet theory and perturbation techniques are used to analyze a classical within-host virus model with periodic drug treatment. Both single and multidrug treatment strategies are investigated. Specifically, the effects of both RT-inhibitors and P-inhibitors on the stability of the infection-free steady state are studied. It is found that when both classes of drugs have periodic drug efficacy functions, then shifting the phase of these functions can critically affect the stability of the infection-free steady state. A numerical study is conducted to illustrate the theoretical results and provide additional insights. [ABSTRACT FROM AUTHOR]