A mathematical model and simulation scenarios for T and B cells immune response to severe acute respiratory syndrome-coronavirus-2

Severe acute respiratory syndrome coronavirus is a type 2 highly contagious, and transmissible among humans;the natural human immune response to severe acute respiratory syndrome-coronavirus-2 combines cell-mediated immunity (lymphocyte) and antibody production. In the present study, we analyzed the dynamic effects of adaptive immune system cell activation in the human host. The methodology consisted of modeling using a system of ordinary differential equations;for this model, the equilibrium free of viral infection was obtained, and its local stability was determined. Analysis of the model revealed that lymphocyte activation leads to total pathogen elimination by specific recognition of viral antigens;the model dynamics are driven by the interaction between respiratory epithelial cells, viral infection, and activation of helper T, cytotoxic T, and B lymphocytes. Numerical simulations showed that the model solutions match the dynamics involved in the role of lymphocytes in preventing new infections and stopping the viral spread;these results reinforce the understanding of the cellular immune mechanisms and processes of the organism against severe acute respiratory syndrome-coronavirus-2 infection, allowing the understanding of biophysical processes that occur in living systems, dealing with the exchange of information at the cellular level.

Cell lysis analysis for respiratory viruses through simulation modeling

An ordinary system of differential equations leading to a simulation model is propose as methodological approach to analysis the incidence of infectious-contagious diseases, in this case using SARS-CoV-2 virus as pathogenic model. The dynamics of the model are drive by the interaction between susceptible cells contemplating respiratory epithelial cells and viral infection mediated by two types of lysis response. To perform the simulations, values of some variables and parameters were selected from referenced sources, considering that previous reports suggested that the viral load in the lower respiratory tract might reach its peak in the second week after the beginning of disease symptoms. The scenarios described in the simulations evidence the performance of the cell lysis response from susceptible cells that have been infected. The recommend model shows that an excess response from both the original virus and the mutated virus leads to an increase in the approximate time to control viral infection within the organism. © 2022 Institute of Physics Publishing. All rights reserved.