The COVID-19 pandemic has brought a serious threat to human life safety worldwide. SARS-CoV-2 virus mainly binds to the target cell surface receptor ACE2 (Angiotensin-converting enzyme 2 ) through the S protein expressed on the surface of the virus, resulting in infection of target cells. During this infection process, the target cell ACE2 receptor plays a very important mediating role. In this paper, a delay differential equation model containing the mediated effect of target cell receptor is established according to the mechanism of SARS-CoV-2 virus invasion of target cells, and the global stability of the infection-free equilibrium and the infected equilibrium of the model is obtained by using the basic reproduction number   and constructing the appropriate Lyapunov functional. The expression of the basic reproduction number   intuitively gives the dependence on the expression ratio of the target cell surface ACE2 receptor, which is helpful for the understanding of the mechanism of SARS-CoV-2 virus infection.

Viral replication in a cell culture is described by a delay reaction-diffusion system. It is shown that infection spreads in cell culture as a reaction-diffusion wave, for which the speed of propagation and viral load can be determined both analytically and numerically. Competition of two virus variants in the same cell culture is studied, and it is shown that the variant with larger individual wave speed out-competes another one, and eliminates it. This approach is applied to the Delta and Omicron variants of the SARS-CoV-2 infection in the cultures of human epithelial and lung cells, allowing characterization of infectivity and virulence of each variant, and their comparison.

The 2019 novel coronavirus (COVID-19) emerged at the end of 2019 has a great influence on the health and lives of people all over the world. The spread principle is still unclear. This paper considers a novel evolution model of COVID-19 in terms of an integral-differential equation, involving vaccination effect and the incubation of COVID-19. The proposed mathematical model is rigorously analyzed on its asymptotic behavior with new probability functions, showing the final spread tendency. Moreover, our model is also verified numerically by the practical epidemic data of COVID-19 in Yangzhou from July to August 2021.

We present an early version of a Susceptible-Exposed-Infected-Recovered-Deceased (SEIRD) mathematical model based on partial differential equations coupled with a heterogeneous diffusion model. The model describes the spatio-temporal spread of the COVID-19 pandemic, and aims to capture dynamics also based on human habits and geographical features. To test the model, we compare the outputs generated by a finite-element solver with measured data over the Italian region of Lombardy, which has been heavily impacted by this crisis between February and April 2020. Our results show a strong qualitative agreement between the simulated forecast of the spatio-temporal COVID-19 spread in Lombardy and epidemiological data collected at the municipality level. Additional simulations exploring alternative scenarios for the relaxation of lockdown restrictions suggest that reopening strategies should account for local population densities and the specific dynamics of the contagion. Thus, we argue that data-driven simulations of our model could ultimately inform health authorities to design effective pandemic-arresting measures and anticipate the geographical allocation of crucial medical resources.

In this paper, we present an SEIR epidemic model with infectivity in incubation period and homestead-isolation on the susceptible. We prove that the infection-free equilibrium point is locally and globally asymptotically stable with condition We also prove that the positive equilibrium point is locally and globally asymptotically stable with condition Numerical simulations are employed to illustrate our results. In the absence of vaccines or antiviral drugs for the virus, our results suggest that the governments should strictly implement the isolation system to make every effort to curb propagation of disease during the epidemic.

Randomized longitudinal clinical trials are the gold standard to evaluate the effectiveness of interventions among different patient treatment groups. However, analysis of such clinical trials becomes difficult in the presence of missing data, especially in the case where the study endpoints become difficult to measure because of subject dropout rates or/and the time to discontinue the assigned interventions are different among the patient groups. Here we report on using a validated mathematical model combined with an inverse problem approach to predict the values for the missing endpoints. A small randomized HIV clinical trial where endpoints for most of patients are missing is used to demonstrate this approach.

Many experimental systems in biology, especially synthetic gene networks, are amenable to perturbations that are controlled by the experimenter. We developed an optimal design algorithm that calculates optimal observation times in conjunction with optimal experimental perturbations in order to maximize the amount of information gained from longitudinal data derived from such experiments. We applied the algorithm to a validated model of a synthetic Brome Mosaic Virus (BMV) gene network and found that optimizing experimental perturbations may substantially decrease uncertainty in estimating BMV model parameters.

The nucleated polymerization model is a mathematical framework that has been applied to aggregation and fragmentation processes in both the discrete and continuous setting. In particular, this model has been the canonical framework for analyzing the dynamics of protein aggregates arising in prion and amyloid diseases such as as Alzheimer's and Parkinson's disease. We present an explicit steady-state solution to the aggregate size distribution governed by the discrete nucleated polymerization equations. Steady-state solutions have been previously obtained under the assumption of continuous aggregate sizes; however, the discrete solution allows for direct computation and parameter inference, as well as facilitates estimates on the accuracy of the continuous approximation.

In the context of inverse or parameter estimation problems we demonstrate the use of statistically based model comparison tests in several examples of practical interest. In these examples we are interested in questions related to information content of a particular given data set and whether the data will support a more complicated model to describe it. In the first example we compare fits for several different models to describe simple decay in a size histogram for aggregates in amyloid fibril formation. In a second example we investigate whether the information content in data sets for the pest in cotton fields as it is currently collected is sufficient to support a model in which one distinguishes between nymphs and adults. Finally in a third example with data for patients having undergone an organ transplant, we question whether the data content is sufficient to estimate more than 5 of the fundamental parameters in a particular dynamic model.

We formulated a structured population model with distributed parameters to identify mechanisms that contribute to gene expression noise in time-dependent flow cytometry data. The model was validated using cell population-level gene expression data from two experiments with synthetically engineered eukaryotic cells. Our model captures the qualitative noise features of both experiments and accurately fit the data from the first experiment. Our results suggest that cellular switching between high and low expression states and transcriptional re-initiation are important factors needed to accurately describe gene expression noise with a structured population model.

We developed a series of models for the label decay in cell proliferation assays when the intracellular dye carboxyfluorescein succinimidyl ester (CFSE) is used as a staining agent. Data collected from two healthy patients were used to validate the models and to compare the models with the Akiake Information Criteria. The distinguishing features of multiple decay rates in the data are readily characterized and explained via time dependent decay models such as the logistic and Gompertz models.

We formulate an optimal design problem for the selection of best states to observe and optimal sampling times and locations for parameter estimation or inverse problems involving complex nonlinear nonlinear partial differential systems. An iterative algorithm for implementation of the resulting methodology is proposed.

We formalize an algorithm for solving the L(1)-norm best-fit hyperplane problem derived using first principles and geometric insights about L(1) projection and L(1) regression. The procedure follows from a new proof of global optimality and relies on the solution of a small number of linear programs. The procedure is implemented for validation and testing. This analysis of the L(1)-norm best-fit hyperplane problem makes the procedure accessible to applications in areas such as location theory, computer vision, and multivariate statistics.

We present a general class of cell population models that can be used to track the proliferation of cells which have been labeled with a fluorescent dye. The mathematical models employ fluorescence intensity as a structure variable to describe the evolution in time of the population density of proliferating cells. While cell division is a major component of changes in cellular fluorescence intensity, models developed here also address overall label degradation.

We improve the lower bound on the extremal version of the Maximum Agreement Subtree problem. Namely we prove that two binary trees on the same n leaves have subtrees with the same ≥ c log log n leaves which are homeomorphic, such that homeomorphism is identity on the leaves.

There are two simple solutions to reaction-diffusion systems with limit-cycle reaction kinetics, producing oscillatory behaviour. The reaction parameter mu gives rise to a 'space-invariant' solution, and mu versus the ratio of the diffusion coefficients gives rise to a 'time-invariant' solution. We consider the case where both solution types may be possible. This leads to a refinement of the Turing model of pattern formation. We add convection to the system and investigate its effect. More complex solutions arise that appear to combine the two simple solutions. The convective system sheds light on the underlying behaviour of the diffusive system.