JMB-HEADER RAS-JOURNALS EIMB Pleiades Publishing

RUS

             

ENG

YearIMPACT-FACTOR
2022  1,200
2021  1,540
2020  1,374
2019  1,023
2018  0,932
2017  0,977
2016  0,799
2015  0,662
2014  0,740
2013  0,739
2012  0,637
2011  0,658
2010  0,654
2009  0,570
2008  0,849
2007  0,805
2006  0,330
2005  0,435
2004  0,623
2003  0,567
2002  0,641
2001  0,490
2000  0,477
1999  0,762
1998  0,785
1997  0,507
1996  0,518
1995  0,502
Vol 57(2023) N 4 p. 700-713; DOI 10.1134/S0026893323040076 Full Text

I.A. Gainova1*, A.E. Soboleva2, D.S. Grebennikov3,4, G.A. Bocharov3,4

Mathematical Modeling of HIV Replicaton and the Response of the Interferon System

1Sobolev Institute of Mathematics, Siberian Branch, Russian Academy of Sciences, Novosibirsk, 630090 Russia
2Moscow Institute of Physics and Technology (National Research University), Dolgoprudny, Moscow Region, 141701 Russia
3Marchuk Institute of Numerical Mathematics, Russian Academy of Sciences, Moscow, 119333 Russia
4Sechenov First Moscow State Medical University, Ministry of Health of the Russian Federation, Moscow, 119991 Russia

*gajnova@math.nsc.ru
Received - 2022-08-09; Revised - 2022-11-29; Accepted - 2022-12-24

Developing physiologically meaningful mathematical models that describe multilevel regulation in a complex network of immune processes, in particular, of the system of interferon-regulated virus production processes, is a fundamental scientific problem, within the framework of an interdisciplinary systems approach to research in immunology. Here, we have presented a detailed high-dimensional model describing HIV (human immunodeficiency virus) replication, the response of type I interferon (IFN) to the virus infection of the cell, and suppression of the action of IFN-induced proteins by HIV accessory proteins. As a result, this model includes interactions of all three processes for the first time. The mathematical model is a system of 37 nonlinear ordinary differential equations including 78 parameters. Importantly, the model describes not only the processes of the IFN response of the cell to virus infection, but also the mechanisms used by the virus to prevent effects of the IFN system.

mathematical model, human immunodeficiency virus, replication, accessory proteins, type I interferon, interferon response, interferon-stimulated proteins



JMB-FOOTER RAS-JOURNALS