scholarly journals Optimal control of an HIV model with CTL cells and latently infected cells

2020 ◽  
Vol 10 (2) ◽  
pp. 207-225 ◽  
Author(s):  
Jaouad Danane ◽  
◽  
Karam Allali
Keyword(s):  
Optimal Control ◽  
Hiv Model ◽  
Latently Infected ◽  
Infected Cells

scholarly journals Threshold dynamics of a general delayed HIV model with double transmission modes and latent viral infection

2021 ◽  
Vol 7 (2) ◽  
pp. 2456-2478
Author(s):  
Xin Jiang ◽  
Keyword(s):  
Time Delay ◽  
Threshold Dynamics ◽  
Global Dynamics ◽  
Asymptotically Stable ◽  
Globally Asymptotically Stable ◽  
Hiv Model ◽  
Transmission Modes ◽  
Latently Infected ◽  
Vital Effect ◽  
Infected Cells

<abstract><p>In this paper, a general HIV model incorporating intracellular time delay is investigated. Taking the latent virus infection, both virus-to-cell and cell-to-cell transmissions into consideration, the model exhibits threshold dynamics with respect to the basic reproduction number $ \mathfrak{R}_0 $. If $ \mathfrak{R}_0 &lt; 1 $, then there exists a unique infection-free equilibrium $ E_0 $, which is globally asymptotically stable. If $ \mathfrak{R}_0 &gt; 1 $, then there exists $ E_0 $ and a globally asymptotically stable infected equilibrium $ E^* $. When $ \mathfrak{R}_0 = 1 $, $ E_0 $ is linearly neutrally stable and a forward bifurcation takes place without time delay around $ \mathfrak{R}_0 = 1 $. The theoretical results and corresponding numerical simulations show that the existence of latently infected cells and the intracellular time delay have vital effect on the global dynamics of the general virus model.</p></abstract>

Nonlinear incidence Human immunodeficiency virus infection model with optimal control

2020 ◽  
Vol 34 (11) ◽  
pp. 2050100
Author(s):  
David Yaro ◽  
Aly R. Seadawy ◽  
Dianchen Lu
Keyword(s):  
Optimal Control ◽  
Human Immunodeficiency Virus ◽  
Evolutionary Dynamics ◽  
Control Strategies ◽  
Cellular Level ◽  
Infection Model ◽  
Hiv Model ◽  
Immunodeficiency Virus ◽  
Infected Cells ◽  
Horizontal Spread

Mathematical modeling plays a crucial role in understanding the dynamics of Human immunodeficiency virus (HIV) disease. Most models deal with the vertical and horizontal spread of disease, but few studies have focused on the evolutionary dynamics of HIV at the cellular level. In this paper, we present an HIV model to analyze the dynamics of HIV infection at the cellular level to produce more natural results. We present a detailed stability analysis of disease-free and viral-persistence equilibrium in the system. In addition, sensitivity analysis and optimal control strategies are used to analyze the role of antiretroviral drug therapy and dietary supplements in controlling the concentration of infected cells and viruses.

scholarly journals Optimal control of an HIV model with a trilinear antibody growth function

2021 ◽  
Vol 0 (0) ◽  
pp. 0
Author(s):  
Karam Allali ◽  
Sanaa Harroudi ◽  
Delfim F. M. Torres
Keyword(s):  
Optimal Control ◽  
Nonlinear Differential Equations ◽  
Adaptive Immune Response ◽  
Growth Function ◽  
Optimal Control Strategy ◽  
Hiv Model ◽  
Adaptive Immune ◽  
Immunodeficiency Virus ◽  
Infected Cells ◽  
Disease Free

<p style='text-indent:20px;'>We propose and study a new mathematical model of the human immunodeficiency virus (HIV). The main novelty is to consider that the antibody growth depends not only on the virus and on the antibodies concentration but also on the uninfected cells concentration. The model consists of five nonlinear differential equations describing the evolution of the uninfected cells, the infected ones, the free viruses, and the adaptive immunity. The adaptive immune response is represented by the cytotoxic T-lymphocytes (CTL) cells and the antibodies with the growth function supposed to be trilinear. The model includes two kinds of treatments. The objective of the first one is to reduce the number of infected cells, while the aim of the second is to block free viruses. Firstly, the positivity and the boundedness of solutions are established. After that, the local stability of the disease free steady state and the infection steady states are characterized. Next, an optimal control problem is posed and investigated. Finally, numerical simulations are performed in order to show the behavior of solutions and the effectiveness of the two incorporated treatments via an efficient optimal control strategy.</p>

scholarly journals An HIV model with age-structured latently infected cells

2016 ◽  
Vol 11 (sup1) ◽  
pp. 192-215 ◽  
Author(s):  
Areej Alshorman ◽  
Chathuri Samarasinghe ◽  
Wenlian Lu ◽  
Libin Rong
Keyword(s):  
Hiv Model ◽  
Latently Infected ◽  
Infected Cells ◽  
Age Structured

scholarly journals Mathematical Analysis of the Role of HIV/HBV Latency in Hepatocytes

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Hasifa Nampala ◽  
Matylda Jablonska-Sabuka ◽  
Martin Singull
Keyword(s):  
Optimal Control ◽  
Viral Latency ◽  
Latency Period ◽  
Viral Reservoirs ◽  
Optimal Control Strategy ◽  
Analytical Results ◽  
Latently Infected ◽  
Infected Cells ◽  
Cd4 Cell ◽  
The Impact

The biggest challenge of treating HIV is rampant liver-related morbidity and mortality. This is, to some extent, attributed to hepatocytes acting as viral reservoirs to both HIV and HBV. Viral reservoirs harbour latent provirus, rendering it inaccessible by combinational antiretroviral therapy (cART) that is specific to actively proliferating virus. Latency reversal agents (LRA) such as Shock and kill or lock and block, aiming at activating the latently infected cells, have been developed. However, they are CD4+ cell-specific only. There is evidence that the low replication level of HIV in hepatocytes is mainly due to the latency of the provirus in these cells. LRA are developed to reduce the number of latently infected cells; however, the impact of the period viral latency in hepatocytes especially, during HIV/HBV coinfection, needs to be investigated. Viral coinfection coupled with lifelong treatment of HIV/HBV necessitates investigation for the optimal control strategy. We propose a coinfection mathematical model with delay and use optimal control theory to analyse the effect of viral latency in hepatocytes on the dynamics of HIV/HBV coinfection. Analytical results indicate that HBV cannot take a competitive exclusion against HIV; thus, the coinfection endemic equilibrium implies chronic HBV in HIV-infected patients. Numerical and analytical results indicate that both HIV and HBV viral loads are higher with longer viral latency period in hepatocytes, which indicates the need to upgrade LRA to other non-CD4+ cell viral reservoirs. Higher viral load caused by viral latency coupled with the effects of cART partly explains why liver-related complications are the leading cause of mortality in HIV-infected persons.

scholarly journals Induction of Autophagy to Achieve a Human Immunodeficiency Virus Type 1 Cure

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1798
Author(s):  
Grant R. Campbell ◽  
Stephen A. Spector
Keyword(s):  
Human Immunodeficiency Virus ◽  
Antiretroviral Therapy ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Functional Cure ◽  
Immunodeficiency Virus ◽  
Latently Infected ◽  
Infected Cells ◽  
Hiv 1

Effective antiretroviral therapy has led to significant human immunodeficiency virus type 1 (HIV-1) suppression and improvement in immune function. However, the persistence of integrated proviral DNA in latently infected reservoir cells, which drive viral rebound post-interruption of antiretroviral therapy, remains the major roadblock to a cure. Therefore, the targeted elimination or permanent silencing of this latently infected reservoir is a major focus of HIV-1 research. The most studied approach in the development of a cure is the activation of HIV-1 expression to expose latently infected cells for immune clearance while inducing HIV-1 cytotoxicity—the “kick and kill” approach. However, the complex and highly heterogeneous nature of the latent reservoir, combined with the failure of clinical trials to reduce the reservoir size casts doubt on the feasibility of this approach. This concern that total elimination of HIV-1 from the body may not be possible has led to increased emphasis on a “functional cure” where the virus remains but is unable to reactivate which presents the challenge of permanently silencing transcription of HIV-1 for prolonged drug-free remission—a “block and lock” approach. In this review, we discuss the interaction of HIV-1 and autophagy, and the exploitation of autophagy to kill selectively HIV-1 latently infected cells as part of a cure strategy. The cure strategy proposed has the advantage of significantly decreasing the size of the HIV-1 reservoir that can contribute to a functional cure and when optimised has the potential to eradicate completely HIV-1.

scholarly journals Targeting the latent human cytomegalovirus reservoir for T-cell-mediated killing with virus-specific nanobodies

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Timo W. M. De Groof ◽  
Elizabeth G. Elder ◽  
Eleanor Y. Lim ◽  
Raimond Heukers ◽  
Nick D. Bergkamp ◽  
...  
Keyword(s):  
Gene Expression ◽  
Human Cytomegalovirus ◽  
Early Gene ◽  
Latent Reservoir ◽  
Solid Organ ◽  
Cell Transplant ◽  
Viral Receptor ◽  
Transplant Patients ◽  
Latently Infected ◽  
Infected Cells

AbstractLatent human cytomegalovirus (HCMV) infection is characterized by limited gene expression, making latent HCMV infections refractory to current treatments targeting viral replication. However, reactivation of latent HCMV in immunosuppressed solid organ and stem cell transplant patients often results in morbidity. Here, we report the killing of latently infected cells via a virus-specific nanobody (VUN100bv) that partially inhibits signaling of the viral receptor US28. VUN100bv reactivates immediate early gene expression in latently infected cells without inducing virus production. This allows recognition and killing of latently infected monocytes by autologous cytotoxic T lymphocytes from HCMV-seropositive individuals, which could serve as a therapy to reduce the HCMV latent reservoir of transplant patients.

Galectin-3 is involved in HIV-1 expression through NF-κB activation and associated with Tat in latently infected cells

2019 ◽  
Vol 260 ◽  
pp. 86-93 ◽  
Author(s):  
Mika Okamoto ◽  
Akemi Hidaka ◽  
Masaaki Toyama ◽  
Masanori Baba
Keyword(s):  
Latently Infected ◽  
Galectin 3 ◽  
Infected Cells ◽  
Hiv 1
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