In December 2019, a newly discovered SARS-CoV-2 virus  emerged from China and propagated worldwide as a pandemic , resulting in about 35 percent mortality . In the absence of preventive medicine or a ready to use vaccine, mathematical models can provide useful scientific insights about transmission patterns and targets for drug development. In this study, we propose a within-host mathematical model of SARS-CoV-2 infection considering innate and adaptive immune responses. We analyze the equilibrium points of the proposed model and obtain an expression of the basic reproduction number. We then numerically show the existence of a transcritical bifurcation. The proposed model is calibrated to real viral load data and using the estimated parameters, we perform global sensitivity analysis with respect to the peak of viral load. Finally, we study the efficacy of antiviral drugs and vaccination on the dynamics of SARS-CoV-2 infection. Our results suggest that blocking virus production from infected cells is more effective than reducing the infection rate in terms of decrease in viral load . Vaccination is also found useful but during the vaccine development phase, blocking virus production from infected cells can be targeted for antiviral drug development.
In December 2019, a newly discovered SARS-CoV-2 virus was emerged from China and propagated worldwide as a pandemic . In the absence of preventive medicine or a ready to use vaccine, mathematical models can provide useful scientific insights about transmission patterns and targets for drug development. In this study, we propose a within-host mathematical model of SARS-CoV-2 infection considering innate and adaptive immune responses. We analyze the equilibrium points of the proposed model and obtain an expression of the basic reproduction number. We then numerically show the existence of a transcritical bifurcation. The proposed model is calibrated to real viral load data of two COVID-19 patients. Using the estimated parameters, we perform global sensitivity analysis with respect to the peak of viral load. Finally, we study the efficacy of antiviral drugs and vaccination on the dynamics of SARS-CoV-2 infection. Our results suggest that blocking the production of the virus by infected cells decreases the viral load more than reducing the infection rate of healthy cells . Vaccination is also found useful but during the vaccine development phase, blocking virus production from infected cells can be targeted for antiviral drug development.
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was
D
, resulting in about 35 percent mortality
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and using
of two COVID-19 patients. Using
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virus production from infected cells is more effective
the production of the virus by infected cells decreases the viral load more
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in terms of decrease in viral load
of healthy cells