Abstract
We focus on the importance of pyroptosis and superinfection on the maintenance of thehuman immunodeficiency virus (HIV) latent reservoir on infected patients. The latent reservoir hasbeen found to be crucial to the persistence of low levels of viral loads found in HIV-infected patients,after many years of successfully suppressive anti-retroviral therapy (ART). This reservoir seems to actas an archive for strains of HIV no longer dominant in the blood, such as wild-type virus. When apatient decides to quit therapy there is a rapid turnover and the wild-type virus re-emerges. Thus, itis extremely important to understand the mechanisms behind the maintenance of this reservoir. Forthat, we propose a fractional order model for the dynamics of HIV, where pyroptosis and superinfectionare considered. The model is simulated for biological meaningful parameters and interesting patternsare found. Our results are interpreted for clinical appreciation.
Highlights
human immunodeficiency virus (HIV) is associated with impairment and destruction of the immune system’s response, mostly by depletion of CD4+ T cells
In 2006, Kim et al [4] study the factors influencing the persistence of the latent reservoir and of low viral load in HIV infected patients, under antiretroviral therapy (ART)
In 2009, Rong et al [5] review several mathematical models for HIV dynamics proposed in the literature
Summary
HIV is associated with impairment and destruction of the immune system’s response, mostly by depletion of CD4+ T cells. In 2006, Kim et al [4] study the factors influencing the persistence of the latent reservoir and of low viral load in HIV infected patients, under antiretroviral therapy (ART). In 2009, Rong et al [5] review several mathematical models for HIV dynamics proposed in the literature They focus on the quantitative events underlying HIV latency, on the reservoir stability, on the low-level viremia persistence and on the emergence of intermittent viral blips. In 2015, Wang et al [6] develop a mathematical model to study the pyroptosis mechanism, a programmed cell death, and show how pyroptosis explains the slow time scale of CD4+ T cells depletion and its contribution to the persistence of latently infected cells. Abortative infections, higher activation status of cells due to high virus load, the carrying capacity of the latent reservoir
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