Abstract
The aim of the present paper is to formulate two new mathematical models to describe the co-dynamics of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and human T-cell lymphotropic virus type-I (HTLV-I) in a host. The models characterizes the interplaying between seven compartments, uninfected ECs, latently SARS-CoV-2-infected ECs, actively SARS-CoV-2-infected ECs, free SARS-CoV-2 particles, uninfected CD4(+)T cells, latently HTLV-I-infected CD4(+)T cells and actively HTLV-I-infected CD4(+)T cells. The models incorporate five intracellular time delays: (i) two delays in the formation of latently SARS-CoV-2-infected ECs and latently HTLV-I-infected CD4(+)T cells, (ii) two delays in the reactivation of latently SARS-CoV-2-infected ECs and latently HTLV-I-infected CD4(+)T cells, and (iii) maturation delay of new SARS-CoV-2 virions. We consider discrete-time delays and distributed-time delays in the first and second models, respectively. We first investigate the properties of the model's solutions, then we calculate all equilibria and study their global stability. The global asymptotic stability is examined by constructing Lyapunov functionals. The analytical findings are supported via numerical simulation. The impact of time delays on the coinfection progression is discussed. We found that, increasing time delays values can have an antiviral treatment-like impact. Our developed coinfection model can contribute to understand the SARS-CoV-2 and HTLV-I co-dynamics and help to select suitable treatment strategies for COVID-19 patients with HTLV-I.