We formulated a novel cellular automata (CA) model for HIV dynamics and drug treatment. The model is built upon realistic biological processes, including the virus replication cycle and mechanisms of drug therapy. Viral load, its effect on infection rate, and the role of latently infected cells in sustaining HIV infection are among the aspects that are explored and incorporated in the model. We assume that the calculation of the number of cells in the neighborhood which influences the center cell's state is based on the viral load. This variable-cell neighborhood enables the simulation of an infection rate that is correlated to the viral load. This approach leads to a new and flexible way of modeling HIV dynamics and allows for the simulation of different antiretroviral drug treatments based on their individual and combined effects. The results of the simulation show the three phases of HIV dynamics (acute, chronic, and AIDS) and the additional drug response phase when drug treatment is added. The dynamics from the model qualitatively match clinical data. Drug treatment combinations with reverse transcriptase inhibitors and protease inhibitors are simulated using various drug efficacies. The results indicate that the model can be very useful in evaluating different drug therapy regimens.
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http://dx.doi.org/10.1016/j.jtbi.2007.11.005 | DOI Listing |
Infect Dis Model
June 2025
Infectious Disease Epidemiology Group, Weill Cornell Medicine-Qatar, Cornell University, Doha, Qatar.
We aimed to understand to what extent knowledge of the prevalence of one sexually transmitted infection (STI) can predict the prevalence of another STI, with application for men who have sex with men (MSM). An individual-based simulation model was used to study the concurrent transmission of HIV, HSV-2, chlamydia, gonorrhea, and syphilis in MSM sexual networks. Using the model outputs, 15 multiple linear regression models were conducted for each STI prevalence, treating the prevalence of each as the dependent variable and the prevalences of up to four other STIs as independent variables in various combinations.
View Article and Find Full Text PDFSubst Use Misuse
January 2025
Division of Allergy and Infectious Diseases, Department of Medicine, University of Washington, Seattle, Washington, USA.
Syringe services programs (SSPs) provide critical evidence-based public health services that decrease harms from drug use for people who use drugs (PWUD). Many SSPs have experienced significant and evolving COVID-19-related disruptions. We aimed to characterize the impacts of COVID-19 on SSP operations in the United States approximately two years into the pandemic.
View Article and Find Full Text PDFClin Pharmacol Ther
January 2025
Certara Predictive Technologies Division, Certara UK Limited, Sheffield, UK.
Understanding cytokine-related therapeutic protein-drug interactions (TP-DI) is crucial for effective medication management in conditions characterized by elevated inflammatory responses. Recent FDA and ICH guidelines highlight a systematic, risk-based approach for evaluating these interactions, emphasizing the need for a thorough mechanistic understanding of TP-DIs. This study integrates the physiologically based pharmacokinetic (PBPK) model for TP (specifically interleukin-6, IL-6) with small-molecule drug PBPK models to elucidate cytokine-related TP-DI mechanistically.
View Article and Find Full Text PDFJ Chem Inf Model
January 2025
State Key Laboratory of Microbial Metabolism, Joint International Research Laboratory of Metabolic & Developmental Sciences and School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai 200030, P.R. China.
The rise of resistance to antiretroviral drugs due to mutations in human immunodeficiency virus-1 (HIV-1) protease is a major obstacle to effective treatment. These mutations alter the drug-binding pocket of the protease and reduce the drug efficacy by disrupting interactions with inhibitors. Traditional methods, such as biochemical assays and structural biology, are crucial for studying enzyme function but are time-consuming and labor-intensive.
View Article and Find Full Text PDFMath Biosci Eng
December 2024
Department of Engineering and Natural Sciences, University of Applied Sciences Merseburg, Eberhard-Leibnitz-Str. 2, D-06217 Merseburg, Germany.
In this article, we reconsider the classical target cell limited dynamical within-host HIV model, solely taking into account the interaction between $ {\rm{CD}}4^{+} $ T cells and virus particles. First, we summarize some analytical results regarding the corresponding dynamical system. For that purpose, we proved some analytical results regarding the system of differential equations as our first main contribution.
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