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Latently infected CD 4 + T cells represent one of the major obstacles to HIV eradication even after receiving prolonged highly active anti-retroviral therapy (HAART). Long-term use of HAART causes the emergence of drug-resistant virus which is then involved in HIV transmission. In this paper, we develop mathematical HIV models with staged disease progression by incorporating entry inhibitor and latently infected cells. We find that entry inhibitor has the same effect as protease inhibitor on the model dynamics and therefore would benefit HIV patients who developed resistance to many of current anti-HIV medications. Numerical simulations illustrate the theoretical results and show that the virus and latently infected cells reach an infected steady state in the absence of treatment and are eliminated under treatment whereas the model including homeostatic proliferation of latently infected cells maintains the virus at low level during suppressive treatment. Therefore, complete cure of HIV needs complete eradication of latent reservoirs. [ABSTRACT FROM AUTHOR]

HIV is a virus that weakens a person's immune system. HIV has three stages, and AIDS is the most severe stage of HIV (Stage 3). People with HIV should take medicine (called ART) recommended by WHO as soon as possible to reduce the amount of virus in the body. In this paper, we formulate a mathematical model for HIV/AIDS with a new approach by focusing on two groups of infectious individuals, HIV and AIDS. We also introduce a controlled class (treated patients and being monitored), and people in this class can spread the disease. We further investigate the essential dynamics of the model through an equilibrium analysis. Optimal control theory is applied to explore effective treatment strategies by combining two control measures: standard antiretroviral therapy and AIDS treatments. Numerical simulation results show the effects of the two time-dependent controls, and they can be used as guidelines for public health interventions. [ABSTRACT FROM AUTHOR]

This paper aims to analyse stability and Hopf bifurcation of the HIV-1 model with immune delay under the functional response of the Holling II type. The global stability analysis has been considered by Lyapunov–LaSalle theorem. And stability and the sufficient condition for the existence of Hopf Bifurcation of the infected equilibrium of the HIV-1 model with immune response are also studied. Some numerical simulations verify the above results. Finally, we propose a novel three dimension system to the future study. [ABSTRACT FROM AUTHOR]

In this paper, with eclipse stage in consideration, we propose an HIV-1 infection model with a general incidence rate and CTL immune response. We first study the existence and local stability of equilibria, which is characterized by the basic infection reproduction number R 0 and the basic immunity reproduction number R 1 . The local stability analysis indicates the occurrence of transcritical bifurcations of equilibria. We confirm the bifurcations at the disease-free equilibrium and the infected immune-free equilibrium with transmission rate and the decay rate of CTLs as bifurcation parameters, respectively. Then we apply the approach of Lyapunov functions to establish the global stability of the equilibria, which is determined by the two basic reproduction numbers. These theoretical results are supported with numerical simulations. Moreover, we also identify the high sensitivity parameters by carrying out the sensitivity analysis of the two basic reproduction numbers to the model parameters. [ABSTRACT FROM AUTHOR]

HIV continues to be a major global health issue, having claimed millions of lives in the last few decades. While several empirical studies support the fact that proper nutrition is useful in the fight against HIV, very few studies have focused on developing and using mathematical modelling approaches to assess the association between HIV, human immune response to the disease, and nutrition. We develop a within-host model for HIV that captures the dynamic interactions between HIV, the immune system and nutrition. We find that increased viral activity leads to increased serum protein levels. We also show that the viral production rate is positively correlated with HIV viral loads, as is the enhancement rate of protein by virus. Although our numerical simulations indicate a direct correlation between dietary protein intake and serum protein levels in HIV-infected individuals, further modelling and clinical studies are necessary to gain comprehensive understanding of the relationship. [ABSTRACT FROM AUTHOR]

A multi-patch HIV/AIDS model with heterosexual transmission is formulated to investigate the impact of population migration on the spread of HIV/AIDS. We derive the basic reproduction number $ R_{0} $ R 0 and prove that if $ R_{0} \lt 1 $ R 0 < 1 , the disease-free equilibrium is globally asymptotically stable. If $ R_{0} \gt 1 $ R 0 > 1 and certain conditions are satisfied, the endemic equilibrium is globally asymptotically stable. We apply the model to two patches and conduct numerical simulations. If HIV/AIDS becomes extinct in each patch when two patches are isolated, the disease remains extinct in two patches when the population migration occurs; if HIV/AIDS spreads in each patch when two patches are isolated, the disease remains persistent in two patches when the population migration occurs; if the disease disappears in one patch and spreads in the other patch when they are isolated, the disease can spread or disappear in two patches if migration rates of individuals are suitably chosen. [ABSTRACT FROM AUTHOR]