HIV-1 infection typically involves a long clinical latency stage during which CD4 counts decline slowly. For the later part of the clinical latency stage it was found recently that this is a highly dynamic phase characterized by rapid turnover rates. Clinical latency can therefore be considered as a quasi-equilibrium state in which CD4 and HIV-1 turnover are in almost perfect balance. Here we consider this quasi-equilibrium to be the stable steady state of a simple host-parasite model in which the parasite (HIV-1) level is determined by the availability of infectable hosts (activated CD4+ T cells). Such models adequately account for the clinical data on the evolution of drug resistant mutants appearing after the administration of anti-HIV d...
In this work, we formulated a mathematical model to study the interaction between HIV/AIDS and Clust...
Acquired Immuno-Deficiency Syndrome (AIDS) is a dreaded outcome of HIV (Human Immunodeficiency Virus...
In this paper, we propose and discuss a possible mechanism, which, via continuous mutations and evol...
In HIV infection, the latent cells represent a reservoir that contributes to the failure of the High...
Latently infected CD 4 + T cells represent one of the major obstacles to HIV eradication even after ...
In HIV infection, the latent cells represent a reservoir that contribute to the of failure of the Hi...
Treatment of human immunodeficiency virus type 1 (HIV-1) infection during the symptomatic phase has ...
Objectives: To investigate factors that may influence the success or failure of powerful antiretrovi...
Treatment of human immunodeficiency virus type 1 (HIV-1) infection during the symptomatic phase has ...
In this paper we propose a model for the dynamics of HIV epidemics under distinct HAART regimes, and...
To understand the role of qualitative differences in multidrug chemotherapy for human immunodeficien...
Treatment of human immunodeficiency virus type 1 (HIV-1) infection during the clinical latency phase...
In this paper we study a delay mathematical model for the dynamics of HIV in HIV-specific CD4 + T he...
In this research, generalized mathematical models depicting HIV-1 pathophysiodynamics are constructe...
Mathematical models provide a means to understand the human immunodeficiency virus (HIV)-infected im...
In this work, we formulated a mathematical model to study the interaction between HIV/AIDS and Clust...
Acquired Immuno-Deficiency Syndrome (AIDS) is a dreaded outcome of HIV (Human Immunodeficiency Virus...
In this paper, we propose and discuss a possible mechanism, which, via continuous mutations and evol...
In HIV infection, the latent cells represent a reservoir that contributes to the failure of the High...
Latently infected CD 4 + T cells represent one of the major obstacles to HIV eradication even after ...
In HIV infection, the latent cells represent a reservoir that contribute to the of failure of the Hi...
Treatment of human immunodeficiency virus type 1 (HIV-1) infection during the symptomatic phase has ...
Objectives: To investigate factors that may influence the success or failure of powerful antiretrovi...
Treatment of human immunodeficiency virus type 1 (HIV-1) infection during the symptomatic phase has ...
In this paper we propose a model for the dynamics of HIV epidemics under distinct HAART regimes, and...
To understand the role of qualitative differences in multidrug chemotherapy for human immunodeficien...
Treatment of human immunodeficiency virus type 1 (HIV-1) infection during the clinical latency phase...
In this paper we study a delay mathematical model for the dynamics of HIV in HIV-specific CD4 + T he...
In this research, generalized mathematical models depicting HIV-1 pathophysiodynamics are constructe...
Mathematical models provide a means to understand the human immunodeficiency virus (HIV)-infected im...
In this work, we formulated a mathematical model to study the interaction between HIV/AIDS and Clust...
Acquired Immuno-Deficiency Syndrome (AIDS) is a dreaded outcome of HIV (Human Immunodeficiency Virus...
In this paper, we propose and discuss a possible mechanism, which, via continuous mutations and evol...