https://doi.org/10.1140/epjp/s13360-025-06475-x
Regular Article
Stability of an HIV-1 abortive infection model with antibody immunity and delayed inflammatory cytokine production
1
Department of Mathematics, Faculty of Science, King Abdulaziz University, P.O. Box 80203, 21589, Jeddah, Saudi Arabia
2
Department of Mathematics, Faculty of Science, Al-Azhar University, Assiut Branch, Assiut, Egypt
Received:
21
March
2025
Accepted:
24
May
2025
Published online:
20
June
2025
HIV-1 remains one of the leading causes of mortality worldwide, primarily targeting CD4
T cells, which are essential for immune defense. A defining characteristic of HIV-1 infection is the gradual depletion of CD4 T cells. Pyroptosis, an intensely inflammatory type of programmed cell death, plays a crucial role in driving disease progression. Mathematical modeling is a powerful tool for examining HIV-1 dynamics and the role of pyroptosis in infection. This work aims to develop and analyze an HIV-1 infection model incorporating pyroptosis, time delay, and antibody-mediated immunity. The model distinguishes between two types of infected CD4 T cells: productively and abortively infected cells. The model incorporates four types of distributed delays: (i) the delay in the development of abortively infected cells, (ii) the delay in the generation of productively infected cells, (iii) the delay in the activation process of inflammatory cytokines, and (iv) the delay in the maturation of newly produced virions. Utilizing Lyapunov functionals along with LaSalle’s invariance principle, we have demonstrated that the stability of steady states depends entirely on two key threshold values: the basic reproduction number (
) and the antibody immune response activation parameter (
). Along with numerical simulations that validate the stability results, the biological implications are also emphasized. To better understand the key factors influencing HIV-1 infection, a sensitivity analysis of is performed. This study explores the effects of antibody response, inflammatory cytokines, and time delays on HIV-1 progression. The results highlight the crucial role of antibodies in limiting viral spread. It is shown that delay parameters function similarly to antiviral therapy by reducing , and delays in cytokine release also contribute to this reduction and these delays should not be overlooked. The findings suggest that simply lowering may not be enough to eliminate the infection without addressing the impact of cytokine-enhanced viral infection. Additionally, a new observation is made that inflammatory cytokines can elevate antibody levels, a previously unreported phenomenon.
Copyright comment Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.
© The Author(s), under exclusive licence to Società Italiana di Fisica and Springer-Verlag GmbH Germany, part of Springer Nature 2025
Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.
