Dynamics of a diffusive and delayed HIV infection model with impaired immunity and latent cell-to-cell transmission

Hui Miao; Hui Miao

doi:10.3934/math.2026774

AIMS Mathematics

2026, Volume 11, Issue 6: 19011-19030. doi: 10.3934/math.2026774

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Research article

Dynamics of a diffusive and delayed HIV infection model with impaired immunity and latent cell-to-cell transmission

Hui Miao ^,

School of Applied Mathematics, Shanxi University of Finance and Economics, Taiyuan 030006, China

Received: 06 May 2026 Revised: 16 June 2026 Accepted: 24 June 2026 Published: 29 June 2026
MSC : 34D40, 35K57, 92D30

Viral concentrations in plasma can be suppressed by antiviral drugs, yet reactivation of latently infected cells is the main obstacle to total human immunodeficiency virus (HIV) elimination. In this paper, to characterize the within-host dynamics of HIV with impaired immunity, we formulated and analyzed a general HIV infection model involving diffusion and three delays. Uninfected CD4$ ^+ $T cells were at risk of infection when they came into contact with three viral transmission routes, namely virus-to-cell infection, latent cell-to-cell transmission, and cell-to-cell transmission, all characterized by general incidence functions. Viral infection reproduction number was calculated, and the global properties were demonstrated. Numerical simulations were carried out to illustrate the corresponding theoretical results.
- viral infection model,
- latent cell-to-cell transmission,
- diffusion,
- general incidence function,
- global stability
Citation: Hui Miao. Dynamics of a diffusive and delayed HIV infection model with impaired immunity and latent cell-to-cell transmission[J]. AIMS Mathematics, 2026, 11(6): 19011-19030. doi: 10.3934/math.2026774

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Abstract

Viral concentrations in plasma can be suppressed by antiviral drugs, yet reactivation of latently infected cells is the main obstacle to total human immunodeficiency virus (HIV) elimination. In this paper, to characterize the within-host dynamics of HIV with impaired immunity, we formulated and analyzed a general HIV infection model involving diffusion and three delays. Uninfected CD4$ ^+ $T cells were at risk of infection when they came into contact with three viral transmission routes, namely virus-to-cell infection, latent cell-to-cell transmission, and cell-to-cell transmission, all characterized by general incidence functions. Viral infection reproduction number was calculated, and the global properties were demonstrated. Numerical simulations were carried out to illustrate the corresponding theoretical results.

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