Fractional Dynamics of HIV with Source Term for the Supply of New CD4+ T-Cells Depending on the Viral Load via Caputo–Fabrizio Derivative

Human immunodeficiency virus (HIV) is a life life-threatening and serious infection caused by a virus that attacks CD4+ T-cells, which fight against infections and make a person susceptible to other diseases. It is a global public health problem with no cure; therefore, it is highly important to study and understand the intricate phenomena of HIV. In this article, we focus on the numerical study of the path-tracking damped oscillatory behavior of a model for the HIV infection of CD4+ T-cells. We formulate fractional dynamics of HIV with a source term for the supply of new CD4+ T-cells depending on the viral load via the Caputo–Fabrizio derivative. In the formulation of fractional HIV dynamics, we replaced the constant source term for the supply of new CD4+ T-cells from the thymus with a variable source term depending on the concentration of the viral load, and introduced a term that describes the incidence of the HIV infection of CD4+ T-cells. We present a novel numerical scheme for fractional view analysis of the proposed model to highlight the solution pathway of HIV. We inspect the periodic and chaotic behavior of HIV for the given values of input factors using numerical simulations.

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Niveau des CD4+ CD38+ HLA-DR+ comme évolution des biomarqueurs de l'infection par le VIH indépendamment de la thérapie antirétrovirale

Batna Journal of Medical Sciences (BJMS) ◽

10.48087/bjmsoa.2017.4206 ◽

2017 ◽

Vol 4 (2) ◽

pp. 155-158

Author(s):

Yanis Meddour ◽

◽

Imène Zerrouk ◽

Fatma Zohra Souid ◽

Mohamed Amine ◽

...

Keyword(s):

T Cells ◽

Viral Load ◽

Hiv Infection ◽

Cd4 T Cells ◽

Therapy Response ◽

Activation Markers ◽

Color Flow ◽

Disease Evolution ◽

Cytokines And Chemokines ◽

Hla Dr

Introduction. HIV infection is characterized by an enhanced synthesis of cytokines and chemokines, a quantitative T cells disequilibrium and increased Turn over that signs a chronic activation of the immune system. Phenotype change in CD4+ T cells by over-expression of activation antigens CD38 and HLA-DR are suggested as markers of this process. Materials and methods. We investigated by four-color flow cytometry the expression of both activation markers on peripheral CD4+ T cells in 106 HIV-1 Algerian infected patients and 34 uninfected controls. Percentage’s expression of CD4+CD38+HLA-DR+ cells was compared with clinical stages, viral load and anti-retroviral treatment (ARV). Results. The proportion of CD4+ T cells coexpressing HLA-DR and CD38 was higher in infected patients than in controls (respectively, 14.2 % ± 3.6 vs. 5.8 % ± 4.1, P=0.01), in symptomatic HIV patients than asymptomatic (13 % ± 3 vs. 15.9 % ± 4.6, P=0.01) and followed viral load kinetics. In matched treated and untreated patients, activated CD4+T proportion does not show any statical difference (respectively, 13 % and 14 %, p=0.09). Conclusion. In our cohort, CD4+ T cells expressing CD38 and HLA-DR were associated with HIV infection and correlated with disease progression, regardless of ARV treatment. As CD4+ count and viral load, this lymphocyte subset may be an interesting disease evolution marker; its value remains to be determined in prognostic or as therapy response indicator.

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A Numerical Study on a Model for HIV Infection of CD4+T-cells by Shifted Chebyshev Polynomials

International Journal Bioautomation ◽

10.7546/ijba.2019.23.2.000498 ◽

2019 ◽

Vol 23 (2) ◽

pp. 163-174

Author(s):

Kourosh Parand ◽

◽

Mohammad Mahdi Moayeri ◽

Sobhan Latifi ◽

◽

...

Keyword(s):

T Cells ◽

Hiv Infection ◽

Chebyshev Polynomials ◽

Cd4 T Cells ◽

Numerical Study

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Mathematical Models of the Complete Course of HIV Infection and AIDS

Journal of Theoretical Medicine ◽

10.1080/1027366021000051772 ◽

2002 ◽

Vol 4 (4) ◽

pp. 215-221 ◽

Cited By ~ 19

Author(s):

R. Paul Duffin ◽

Richard H. Tullis

Keyword(s):

T Cells ◽

Viral Load ◽

T Cell ◽

Hiv Infection ◽

Mathematical Models ◽

Cd4 T Cells ◽

Opportunistic Infections ◽

Viral Clearance ◽

Viral Production ◽

Reservoir Models

Mathematical models of HIV infection are important to our understanding of AIDS. However, most models do not predict both the decrease in CD4+ T cells and the increase in viral load seen over the course of infection. By including terms for continuous loss of CD4+ T cells and incorporating alteration in viral clearance and viral production, two new models have been created that accurately predict the dynamics of the disease. The first model is a clearance rate reduction model and is based on a 10% per year decrease in both viral clearance and CD4+ T cell levels. A macrophage reservoir model incorporating the observation that macrophage viral production increases up to 1000 fold in the presence of opportunistic infections that become increasingly common as disease progresses. Both viral clearance and macrophage reservoir models predict the expected decrease in T cell levels and rise in viral load observed at the onset of AIDS.

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Faculty Opinions recommendation of Transcription factor FOXO3a controls the persistence of memory CD4(+) T cells during HIV infection.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1104534.569097 ◽

2008 ◽

Author(s):

Vicente Planelles

Keyword(s):

T Cells ◽

Transcription Factor ◽

Hiv Infection ◽

Cd4 T Cells ◽

Memory Cd4 T Cells

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Faculty Opinions recommendation of Autocrine production of beta-chemokines protects CMV-Specific CD4 T cells from HIV infection.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1279973.747077 ◽

2009 ◽

Author(s):

Scott Sieg ◽

Nicholas Funderburg

Keyword(s):

T Cells ◽

Hiv Infection ◽

Cd4 T Cells

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Circulating integrin α 4 β 7 + CD4 T cells are enriched for proliferative transcriptional programs in HIV infection

FEBS Letters ◽

10.1002/1873-3468.14163 ◽

2021 ◽

Author(s):

Yashavanth S. Lakshmanappa ◽

Jamin W. Roh ◽

Niharika N. Rane ◽

Ashok R. Dinasarapu ◽

Daphne D. Tran ◽

...

Keyword(s):

T Cells ◽

Hiv Infection ◽

Cd4 T Cells

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Identification of novel genes involved in apoptosis of HIV-infected macrophages using unbiased genome-wide screening

BMC Infectious Diseases ◽

10.1186/s12879-021-06346-7 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Simon X. M. Dong ◽

Frederick S. Vizeacoumar ◽

Kalpana K. Bhanumathy ◽

Nezeka Alli ◽

Cristina Gonzalez-Lopez ◽

...

Keyword(s):

T Cells ◽

Hiv Infection ◽

Respiratory Chain ◽

Cd4 T Cells ◽

Chain Complex ◽

Respiratory Chain Complex ◽

Complex Ii ◽

Genome Wide ◽

Latently Infected ◽

Induced Apoptosis

Abstract Background Macrophages, besides resting latently infected CD4+ T cells, constitute the predominant stable, major non-T cell HIV reservoirs. Therefore, it is essential to eliminate both latently infected CD4+ T cells and tissue macrophages to completely eradicate HIV in patients. Until now, most of the research focus is directed towards eliminating latently infected CD4+ T cells. However, few approaches have been directed at killing of HIV-infected macrophages either in vitro or in vivo. HIV infection dysregulates the expression of many host genes essential for the survival of infected cells. We postulated that exploiting this alteration may yield novel targets for the selective killing of infected macrophages. Methods We applied a pooled shRNA-based genome-wide approach by employing a lentivirus-based library of shRNAs to screen novel gene targets whose inhibition should selectively induce apoptosis in HIV-infected macrophages. Primary human MDMs were infected with HIV-eGFP and HIV-HSA viruses. Infected MDMs were transfected with siRNAs specific for the promising genes followed by analysis of apoptosis by flow cytometry using labelled Annexin-V in HIV-infected, HIV-exposed but uninfected bystander MDMs and uninfected MDMs. The results were analyzed using student’s t-test from at least four independent experiments. Results We validated 28 top hits in two independent HIV infection models. This culminated in the identification of four target genes, Cox7a2, Znf484, Cstf2t, and Cdk2, whose loss-of-function induced apoptosis preferentially in HIV-infected macrophages. Silencing these single genes killed significantly higher number of HIV-HSA-infected MDMs compared to the HIV-HSA-exposed, uninfected bystander macrophages, indicating the specificity in the killing of HIV-infected macrophages. The mechanism governing Cox7a2-mediated apoptosis of HIV-infected macrophages revealed that targeting respiratory chain complex II and IV genes also selectively induced apoptosis of HIV-infected macrophages possibly through enhanced ROS production. Conclusions We have identified above-mentioned novel genes and specifically the respiratory chain complex II and IV genes whose silencing may cause selective elimination of HIV-infected macrophages and eventually the HIV-macrophage reservoirs. The results highlight the potential of the identified genes as targets for eliminating HIV-infected macrophages in physiological environment as part of an HIV cure strategy.

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