Modeling the crossover behavior of the bacterial infection with the COVID-19 epidemics.

To explore the crossover linkage of the bacterial infections resulting from the viral infection, within the host body, a computational framework is developed. It analyzes the additional pathogenic effect of Streptococcus pneumonia, one of the bacteria that can trigger the super-infection mechanism in the COVID-19 syndrome and the physiological effects of innate immunity for the control or eradication of this bacterial infection. The computational framework, in a novel manner, takes into account the action of pro-inflammatory and anti-inflammatory cytokines in response to the function of macrophages. A hypothetical model is created and is transformed to a system of non-dimensional mathematical equations. The dynamics of three main parameters (macrophages sensitivity κ , sensitivity to cytokines η and bacterial sensitivity ϵ ), analyzes a "threshold value" termed as the basic reproduction number R 0 which is based on a sub-model of the inflammatory state. Piece-wise differentiation approach is used and dynamical analysis for the inflammatory response of macrophages is studied in detail. The results shows that the inflamatory response, with high probability in bacterial super-infection, is concomitant with the COVID-19 infection. The mechanism of action of the anti-inflammatory cytokines is discussed during this research and it is observed that these cytokines do not prevent inflammation chronic, but only reduce its level while increasing the activation threshold of macrophages. The results of the model quantifies the probable deficit of the biological mechanisms linked with the anti-inflammatory cytokines. The numerical results shows that for such mechanisms, a minimal action of the pathogens is strongly amplified, resulting in the "chronicity" of the inflammatory process.