Analysis of CD4+ T cells in HIV-1 infection model combined with RTI and PI treatments
DOI:
https://doi.org/10.11113/mjfas.v16n2.1634Keywords:
HIV-1 infection, CD4 T cells, stability, RTI, PIAbstract
HIV (Human Immunodeficiency Virus) is a retrovirus that attacks the immune system and subsequently leading to AIDS (Acquired Immunodeficiency Syndrome). CD4+ T cells are among the immune systems destroyed by HIV. The HIV transmission from cell to cell is an infection process of spreading HIV-1 infection. The study developed a mathematical model by considering the contact between HIV-1-infected CD4+ T cells and healthy CD4+ T cells, incorporating antiretroviral treatment. The stability of equilibriums for the model was studied. The local stability for disease-free equilibrium and the global stability for endemic equilibrium were studied. Numerical simulations were presented to examine the implication of antiretroviral therapy. Simulation results showed that reverse transcriptase inhibitor (RTI) therapy was more effective compared to protease inhibitor (PI) therapy in increasing the number of healthy CD4+ T cells.
References
Adams, B. M., Banks, H. T., Davidian, M., Kwon, H. D, Tran, H. T., Wynne, S. N., Rosenberg, E. S. 2005. HIV dynamics: Modeling, data analysis, and optimal treatment protocols. J. Comp. App. Math. 184, 1, 10-49.
Bonhoeffer, S., Coffin, J. M., Nowak, M. A. 1997. Human immunodeficiency virus drug therapy and virus load. J. Virol. 71, 4, 3275-3278.
Chirove, F., Sutimin, Soewono, E., Nuraini, N. 2014. Analysis of combined Langerhans and CD4+ T cells HIV infection. SIAM J. Appl. Math. 74, 4, 1174-1193.
Diekmann, O., Heesterbeek, J. A. P. 2000. Mathematical epidemiology of infectious diseases: Model building, analysis and interpretation. John Wiley & Sons, Chichester, UK.
Hladik, F., Sakchalathorn P., Ballweber, L., Lentz, G., Fialkow, M., Eschenbach, D., McElrath, M. J. 2007. Initial events in establishing vaginal entry and infection by human immunodeficiency virus type-1. Immunity. 26, 2, 257-270.
Jolly, C. 2011. Cell-to-cell transmission of retroviruses: Innate immunity and interferon-induced restriction factors. Virology. 411, 2, 251-259.
Kirchhoff, F. 2013. HIV life cycle: Overview. Encyclopedia of AIDS, 1-9.
Kirschner, D. 1996. Using mathematics to understand HIV immune dynamics. Notices Amer. Math. Soc. 43, 191-202.
Klimas, N., Koneru, A. O., Fletcher, M. A. 2008. Overview of HIV. Psy. Med. 70, 523-530.
Perelson, A. S., Kirschner, D. E., Boer, R. D. 1993. Dynamics of HIV infection of CD4+ T cells. Math. Bio. 114, 1, 81-125.
Sattentau, Q. J. 2010. Cell-to-cell spread of retroviruses. Viruses. 2, 6, 1306--1321.
Srivastava, P. K., Banerjee, M., Chandra, P. Modeling the Drug Therapy for HIV Infection. 2009. J. Biol. Sys. 17, 2, 213-223.
Stafford, M. A., Corey, L., Cao, Y., Daar, E. S., Ho, D. D. and Perelson, A. S. 2000. Modeling plasma virus concentration during primary HIV infection. J. Theor. Bio. 203, 285-301.
Sutimin, Chirove, F., Soewono, E., Nuraini, N., Suromo, L. B. 2017. A model incorporating combined RTIs and PIs therapy during early HIV-1 infection. Math. Bio. 285, 102-111.
Sutimin, Nuraini, N., Chirove, F., Suromo, L. B. 2017. Modelling Multiple Dosing with Drug Holiday in Antiretroviral Treatment on HIV-1 Infection. J. Math. Fund. Sci. 49, 1, 1-17.
Swiggard, W. J., O’Doherty, U., McGain, D., Jeyakumar, D., Malim, M. H. 2004. Long HIV type 1 reverse transcripts can accumulate stably within resting CD4+ T cells while short ones are degraded. AIDS Res.
Hum. Retrovir. 20, 285-295.
Tarfulea, N. 2011. A mathematical model for HIV Treatment with time-varying antiretroviral therapy. Int. J. Comp. Math. 88, 15, 3217-3235.
Vatakis, D. N., Kim, S., Kim, N., Chow, S. A., Zack, J. A. 2009. Human immunodeficiency virus integration efficiency and site selection in quiescent CD4+ T cells. J. Virol., 83, 12, 6222-6233.
Zack, J. A., Arrigo, S. J., Weitsman, S. R., Go, A. S., Haislip, A., Chen, I. S. Y. 1990. HIV-1 entry into quiescent primary lymphocytes: Molecular analysis reveals a labile, latent viral structure. Cell. 61, 2, 213-222.