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<p>Influenza and COVID-19 are two respiratory diseases that cause significant illness and death. Influenza A virus (IAV) is more effective at causing disease compared to types B, C, and D. The novel SARS-CoV-2, or severe acute respiratory syndrome coronavirus 2, is the cause of COVID-19. These two viruses have similar seasonal patterns, symptoms, transmission methods, and immune responses. Several studies have reported many individuals with concurrent infections with both IAV and SARS-CoV-2. Recent works have looked into modeling the co-dynamics of SARS-CoV-2 and IAV, but have not taken cytotoxic T lymphocyte (CTL) immunity into account. This paper investigates the global co-dynamics of IAV and SARS-CoV-2 in vivo, focusing on the role of CTL in killing virus-infected cells during dual infection. Three types of distributed-time delays are included in the suggested model: delay in the emergence of latently infected cells, delay in the activation of latent infected cells, and delay in the maturation of freshly created virions. The model is examined qualitatively, its steady states are computed, and the stability of the steady states is established by using the Lyapunov method, and the outcomes are illustrated through simulations. The impact of CTL immunity on the IAV and SARS-CoV-2 dual infection is discussed. Our results imply that while CTL immunity is essential for preventing SARS-CoV-2 and IAV dual infection, it may also allow both viruses to coexist in specific situations. Additionally, the study discusses how time delays influence the dynamics of dual infection, noting that extended delays can have effects similar to those of antiviral treatments. A long enough delay causes the virus to evolve more slowly, controlling and eventually eliminating the dual infection. This provides us with some recommendations for novel medications that could extend the duration of latent infection, reactivation, or maturation of newly generated virions. Various clinical phenomena, including viral clearance, viral interference, and coexistence of two types of viruses, can be observed using our proposed model.</p>

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Co-dynamics of influenza and COVID-19 with CTL immunity

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月13日

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  • Aeshah A. Raezah,
  • A. M. Elaiw,
  • R. S. Alsulami

摘要

Influenza and COVID-19 are two respiratory diseases that cause significant illness and death. Influenza A virus (IAV) is more effective at causing disease compared to types B, C, and D. The novel SARS-CoV-2, or severe acute respiratory syndrome coronavirus 2, is the cause of COVID-19. These two viruses have similar seasonal patterns, symptoms, transmission methods, and immune responses. Several studies have reported many individuals with concurrent infections with both IAV and SARS-CoV-2. Recent works have looked into modeling the co-dynamics of SARS-CoV-2 and IAV, but have not taken cytotoxic T lymphocyte (CTL) immunity into account. This paper investigates the global co-dynamics of IAV and SARS-CoV-2 in vivo, focusing on the role of CTL in killing virus-infected cells during dual infection. Three types of distributed-time delays are included in the suggested model: delay in the emergence of latently infected cells, delay in the activation of latent infected cells, and delay in the maturation of freshly created virions. The model is examined qualitatively, its steady states are computed, and the stability of the steady states is established by using the Lyapunov method, and the outcomes are illustrated through simulations. The impact of CTL immunity on the IAV and SARS-CoV-2 dual infection is discussed. Our results imply that while CTL immunity is essential for preventing SARS-CoV-2 and IAV dual infection, it may also allow both viruses to coexist in specific situations. Additionally, the study discusses how time delays influence the dynamics of dual infection, noting that extended delays can have effects similar to those of antiviral treatments. A long enough delay causes the virus to evolve more slowly, controlling and eventually eliminating the dual infection. This provides us with some recommendations for novel medications that could extend the duration of latent infection, reactivation, or maturation of newly generated virions. Various clinical phenomena, including viral clearance, viral interference, and coexistence of two types of viruses, can be observed using our proposed model.