IN-VIVOMATHEMATICAL STUDY OF CO-INFECTION DYNAMICS OF HIV-1 ANDMYCOBACTERIUM TUBERCULOSIS

2008 ◽  
Vol 16 (03) ◽  
pp. 357-394 ◽  
Author(s):  
GESHAM MAGOMBEDZE ◽  
WINSTON GARIRA ◽  
EDDIE MWENJE

Human Immunodeficiency Virus type-1 (HIV-1) fuels the pathogenesis of Mycobacterium tuberculosis (Mtb) in humans. We develop a mathematical model in an attempt to understand the immune mechanisms that are involved during the co-infection of Mtb and HIV-1. Our study reveals that infection of an Mtb infected individual with HIV-1 results in fast development of active TB. The mathematical model analysis and simulations show that Mtb infection is linked to HIV infection through macrophages and CD4+ T cells. The study shows that depletion of macrophages and CD4+ T cells by HIV-1 worsens the picture of Mtb infection and in-turn Mtb infection affects the progression of HIV-1 infection since it is also capable of inducing rapid replication of HIV. Our analytical and numerical simulations show that macrophages are a potential reservoir of HIV particles during HIV-1 infection. Co-infection simulations reveal that co-infection exacerbates more the pathogen that caused the first infection. Simulations also show that co-infection disease progression patterns converge to a similar trend after a considerable time interval irrespective of which pathogen first caused infection and the second pathogen that caused co-infection. This work suggests directions for further studies and potential treatment strategies.

2020 ◽  
Vol 13 (06) ◽  
pp. 2050041
Author(s):  
Z. Monfared ◽  
F. Omidi ◽  
Y. Qaseminezhad Raeini

HIV infection is one of the most serious causes of death throughout the world. CD4+ T cells which play an important role in immune protection, are the primary targets for HIV infection. The hallmark of HIV infection is the progressive loss in population of CD4+ T cells. However, the pathway causing this slow T cell decline is poorly understood [16]. This paper studies a discontinuous mathematical model for HIV-1 infection, to investigate the effect of pyroptosis on the disease. For this purpose, we use the theory of discontinuous dynamical systems. In this way, we can better analyze the dynamical behavior of the HIV-1 system. Especially, considering the dynamics of the system on its discontinuity boundary enables us to obtain more comprehensive results rather than the previous researches. A stability region for the system, corresponding to its equilibria on the discontinuity boundary, will be determined. In such a parametric region, the trajectories of the system will be trapped on the discontinuity manifold forever. It is also shown that in the obtained stability region, the disease can lead to a steady state in which the population of uninfected T cells and viruses will preserve at a constant level of cytokines. This means that the pyroptosis will be restricted and the disease cannot progress for a long time. Some numerical simulations based on clinical and experimental data are given which are in good agreement with our theoretical results.


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