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<p>HIV is known for causing the destruction of the immune system by affecting different types of cells, while SARS-CoV-2 is an extremely contagious virus that leads to the development of COVID-19. Understanding how these two viruses interact in coinfected individuals is essential, especially in populations under antiretroviral treatment. In this study, we develop and analyze a novel mathematical model capturing the coinfection dynamics of HIV and SARS-CoV-2 under the influence of highly active antiretroviral therapy (HAART). In contrast to previous models, our formulation includes the effect of HAART on both infections and derives the basic reproduction numbers for each virus. We prove that transcritical bifurcations occur when the basic reproduction numbers cross the threshold value of 1, and we establish the conditions for stability of the disease-free equilibria. Numerical simulations show that HAART, although designed to control HIV, also reduces SARS-CoV-2 proliferation in coinfected hosts, which, as far as we know, has not been fully addressed in previous models in the literature. These findings reveal a potentially beneficial indirect effect of antiretroviral therapy on SARS-CoV-2 dynamics, offering new theoretical insights into the control of viral coinfections.</p>

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Qualitative analysis of HAART effects on HIV and SARS-CoV-2 coinfection model

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月11日

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  • João Paulo Simões Maurício de Carvalho

摘要

HIV is known for causing the destruction of the immune system by affecting different types of cells, while SARS-CoV-2 is an extremely contagious virus that leads to the development of COVID-19. Understanding how these two viruses interact in coinfected individuals is essential, especially in populations under antiretroviral treatment. In this study, we develop and analyze a novel mathematical model capturing the coinfection dynamics of HIV and SARS-CoV-2 under the influence of highly active antiretroviral therapy (HAART). In contrast to previous models, our formulation includes the effect of HAART on both infections and derives the basic reproduction numbers for each virus. We prove that transcritical bifurcations occur when the basic reproduction numbers cross the threshold value of 1, and we establish the conditions for stability of the disease-free equilibria. Numerical simulations show that HAART, although designed to control HIV, also reduces SARS-CoV-2 proliferation in coinfected hosts, which, as far as we know, has not been fully addressed in previous models in the literature. These findings reveal a potentially beneficial indirect effect of antiretroviral therapy on SARS-CoV-2 dynamics, offering new theoretical insights into the control of viral coinfections.