The complexity of the immune responses is a major challenge in current virotherapy. This study incorporates the innate immune response into our basic model for virotherapy and investigates how the innate immunity affects the outcome of virotherapy. The viral therapeutic dynamics is largely determined by the viral burst size, relative innate immune killing rate, and relative innate immunity decay rate. The innate immunity may complicate virotherapy in the way of creating more equilibria when the viral burst size is not too big, while the dynamics is similar to the system without innate immunity when the viral burst size is big.

The complexity of oncolytic virotherapy arises from many factors. In this study, we incorporate environmental noise and stochastic effects to our basic deterministic model and propose a stochastic model for viral therapy in terms of Ito stochastic differential equations. We conduct a detailed analysis of the model using boundary methods. We find two combined parameters, one describes possibilities of eradicating tumors and one is an increasing function of the viral burst size, which serve as thresholds to classify asymptotical dynamics of the model solution paths. We show there are three ergodic invariant probability measures which correspond to equilibrium states of the deterministic model, and extra possibility to eradicate tumor due to strong variance of tumor growth rate and medium viral burst size. Numerical analysis demonstrates several typical solution paths with biological explanations. In addition, we provide some medical interpretations and implications.

In this paper, we consider a system of delay differential equations that models the oncolytic virotherapy on solid tumours with the delay of viral infection in the presence of the innate immune response. We conduct qualitative and numerical analysis, and provide possible medical implications for our results. The system has four equilibrium solutions. Fixed point analysis indicates that increasing the burst size and infection rate of the viruses has positive contribution to the therapy. However, increasing the immune killing infection rate, the immune stimulation rate, or the immune killing virus rate may lead the treatment failed. The viral infection time delay induces backward Hopf bifurcations, which means that the therapy may fail before time delay increases passing through a Hopf bifurcation. The parameter analysis also shows how saddle-node and Hopf bifurcations occur as viral burst size and other parameters vary, which yields further insights into the dynamics of the virotherapy.

Based on our deterministic models for cholera epidemics, we propose a stochastic model for cholera epidemics to incorporate environmental fluctuations which is a nonlinear system of Itô stochastic differential equations. We conduct an asymptotical analysis of dynamical behaviors for the model. The basic stochastic reproduction value ${\mathcal{ℛ}}_s$ is defined in terms of the basic reproduction number $R_0$ for the corresponding deterministic model and noise intensities. The basic stochastic reproduction value determines the dynamical patterns of the stochastic model. When ${\mathcal{ℛ}}_s<1$ , the cholera infection will extinct within finite periods of time almost surely. When ${\mathcal{ℛ}}_s>1$ , the cholera infection will persist most of time, and there exists a unique stationary ergodic distribution to which all solutions of the stochastic model will approach almost surely as noise intensities are bounded. When the basic reproduction number $R_0$ for the corresponding deterministic model is greater than 1, and the noise intensities are large enough such that ${\mathcal{ℛ}}_s<1$ , the cholera infection is suppressed by environmental noises. We carry out numerical simulations to illustrate our analysis, and to compare with the corresponding deterministic model. Biological implications are pointed out.

Glioblastomas are highly malignant brain tumors. Knowledge of growth rates and growth patterns is useful for understanding tumor biology and planning treatment logistics. Based on untreated human glioblastoma data collected in Trondheim, Norway, we first fit the average growth to a Gompertz curve, then find a best fitted white noise term for the growth rate variance. Combining these two fits, we obtain a new type of Gompertz diffusion dynamics, which is a stochastic differential equation (SDE). Newly collected untreated human glioblastoma data in Seattle, US, re-verify our model. Instead of growth curves predicted by deterministic models, our SDE model predicts a band with a center curve as the tumor size average and its width as the tumor size variance over time. Given the glioblastoma size in a patient, our model can predict the patient survival time with a prescribed probability. The survival time is approximately a normal random variable with simple formulas for its mean and variance in terms of tumor sizes. Our model can be applied to studies of tumor treatments. As a demonstration, we numerically investigate different protocols of surgical resection using our model and provide possible theoretical strategies.