This paper presents current knowledge about the structure and function of the lymphatic system. Mathematical models of lymph flow in the single lymphangion, the series of lymphangions, the lymph nodes, and the whole lymphatic system are considered. The main results and further perspectives are discussed.

In this work we develop a model of viral infection in host tissues in order to study the influence of the immune response on the infection spreading speed and on the viral load characterizing, respectively, severity of symptoms and infection transmission rate. Dynamics of the interaction between viral infection and the immune response is studied with nonlocal reaction-diffusion equations for the concentrations of virus, interferon, immune cells and antibodies. Analytical results for infection spreading speed and viral load are completed by numerical simulations. At the first stage, progression of viral infection is confronted by the innate immune response mostly determined by the local interferon production. The modeling results show in this case that infection spreading speed does not depend on interferon concentration, while the total viral load decreases with the increase of its concentration. Next, we consider the influence of globally circulating interferon and show that, in contrast to local interferon diffusion, infection spreading speed decreases with increasing of global interferon level, and the total viral load also decreases. At the next stage, adaptive immune response mediated by antibodies and cytotoxic T cells (CTL) further influences infection progression. In this case, the infection propagation speed and the total viral load are decreased by the immune response. The humoral adaptive response (antibodies) increases the global interferon concentration through the viral load, while the cellular adaptive response (CTL) decreases it.

The problem on a fluid flow in a pulsating vessel is considered in the framework of the quasi-one-dimensional hemodynamic equations. The fluid viscosity is assumed to be anisotropic; i.e., the...

Viral infection spreads in cell culture or tissue as a reaction–diffusion wave. It is characterized by three main parameters: virus replication number, $R_v$, which determines whether infection progresses, wave speed, c, which correlates with the virus virulence, and viral load, $J\left(v\right)$, which determines the infection transmission rate. In this work, we study how the inflammation triggered by viral infection influences its progression. We obtain analytical expressions for $R_v,c$, and $J\left(v\right)$ and show how they depend on the intensity of inflammation characterized by one or two parameters. Analytical and numerical results show that inflammation decreases the viral replication number, virus virulence, and infectivity, though there are different cases depending on the parameters of the model.

A model of lymph flow in the human lymphatic system in the quasi-one-dimensional approach has been created and investigated under different conditions. The model includes an implementation of contractions and valve influence on lymph flow. We consider contractions of lymphatic vessels and their influence on resulting flow in the whole network of lymphatic vessels and lymph nodes. We have investigated flow with zero pressure gradient and have found parameters, which influence the efficiency of contractions most significantly.