Infection with HIV-1, degrading the human immune system and recent advances of drug therapy to arrest HIV-1 infection, has generated considerable research interest in the area. Sebastian Bonhoeffer et al. [2], introduced a population model representing long term dynamics of HIV infection in response to available drug therapies. We consider a similar type of approximate model incorporating time delay in the process of infection on the healthy T cells which, in turn, implies inclusion of a similar delay in the process of viral replication. The model is studied both analytically and numerically. We also include a similar delay in the killing rate of infected CD4 + T cells by Cytotoxic TLymphocyte (CTL) and in the stimulation of CTL and analyze two resulting models numerically.The models with no time delay present have two equilibria: one where there is no infection and a non-trivial equilibrium where the infection can persist. If there is no time delay then the non-trivial equilibrium is locally asymptotically stable. Both our analytical results (for the first model) and our numerical results (for all three models) indicate that introduction of a time delay can destabilize the non-trivial equilibrium. The numerical results indicate that such destabilization occurs at realistic time delays and that there is a threshold time delay beneath which the equilibrium with infection present is locally asymptotically stable and above which this equilibrium is unstable and exhibits oscillatory solutions of increasing amplitude.

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In this research article, we establish a fractional-order mathematical model to explore the infections of the coronavirus disease (COVID-19) caused by the novel SARS-CoV-2 virus. We introduce a set of fractional differential equations taking uninfected epithelial cells, infected epithelial cells, SARS-CoV-2 virus, and CTL response cell accounting for the lytic and non-lytic effects of immune responses. We also include the effect of a commonly used antiviral drug in COVID-19 treatment in an optimal control-theoretic approach. The stability of the equilibria of the fractional ordered system using qualitative theory. Numerical simulations are presented using an iterative scheme in Matlab in support of the analytical results.

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In recent, non-pharmaceutical intervention (lockdown, quarantine, expended testing) and the pharmaceutical intervention (use of commonly used drugs) are the only available strategies to control the COVID-19 disease. Though the scientist all over the world are engaging themselves to find the way out the vaccine of COVID-19, still it is persisted unanswered how to oust the pandemic epidemic from the world. Generally, social distancing, using the mask, etc. are the only available policy to control the pandemic. In this situation uses of common drugs (Azithromycin, HCQ, Antiprotozoal with Doxycycline, Levocetirizine with Montelukast) are common but effective treatment for the reported and hospitalized patient. These drugs activate the immune system of our body to fight against the disease progression. We have formulated a seven compartmental SEIQR type model to explore the COVID-19 disease progression. We have studied the effect of pharmaceutical and non pharmaceutical intervention as a control input and it effect to reduce the number of the infected population while reducing the cost related with the awareness and drug in a specific time frame. Analytical finding tells that the system behavior depends on basic reproduction

COVID-19 is caused by the increase of SARS-CoV-2 viral load in the respiratory system. Epithelial cells in the human lower respiratory tract are the major target area of the SARS-CoV-2 viruses. To fight against the SARS-CoV-2 viral infection, innate and thereafter adaptive immune responses be activated which are stimulated by the infected epithelial cells. Strong immune response against the COVID-19 infection can lead to longer recovery time and less severe secondary complications. We proposed a target cell-limited mathematical model by considering a saturation term for SARS-CoV-2-infected epithelial cells loss reliant on infected cells level. The analytical findings reveal the conditions for which the system undergoes transcritical bifurcation and alternation of stability for the system around the steady states happens. Due to some external factors, while the viral reproduction rate exceeds its certain critical value, backward bifurcation and reinfection may take place and to inhibit these complicated epidemic states, host immune response, or immunopathology would play the essential role. Numerical simulation has been performed in support of the analytical findings.

During the past several years, the deadly COVID-19 pandemic has dramatically affected the world; the death toll exceeds 4.8 million across the world according to current statistics. Mathematical modeling is one of the critical tools being used to fight against this deadly infectious disease. It has been observed that the transmission of COVID-19 follows a fading memory process. We have used the fractional order differential operator to identify this kind of disease transmission, considering both fear effects and vaccination in our proposed mathematical model. Our COVID-19 disease model was analyzed by considering the Caputo fractional operator. A brief description of this operator and a mathematical analysis of the proposed model involving this operator are presented. In addition, a numerical simulation of the proposed model is presented along with the resulting analytical findings. We show that fear effects play a pivotal role in reducing infections in the population as well as in encouraging the vaccination campaign. Furthermore, decreasing the fractional-order parameter α value minimizes the number of infected individuals. The analysis presented here reveals that the system switches its stability for the critical value of the basic reproduction number R0=1.

The current emergence of coronavirus (SARS-CoV-2) puts the world in threat. The structural research on the receptor recognition by SARS-CoV-2 has identified the key interactions between SARS-CoV-2 spike protein and its host (epithelial cell) receptor, also known as angiotensin-converting enzyme 2 (ACE2). It controls both the cross-species and human-to-human transmissions of SARS-CoV-2. In view of this, we propose and analyze a mathematical model for investigating the effect of CTL responses over the viral mutation to control the viral infection when a postinfection immunostimulant drug (pidotimod) is administered at regular intervals. Dynamics of the system with and without impulses have been analyzed using the basic reproduction number. This study shows that the proper dosing interval and drug dose both are important to eradicate the viral infection.