Assessing the impact of SARS-CoV-2 infection on the dynamics of dengue and HIV via fractional derivatives

Omame, Andrew; Abbas, Mujahid; Abdel‐Aty, Abdel‐Haleem

doi:10.1016/j.chaos.2022.112427

Cited by 34 publications

(19 citation statements)

References 41 publications

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“…The symptoms of COVID‐19 vary from mild fever, cough, and myalgia to severe acute respiratory distress syndrome (ARDS) 3–5 . Even though it is rapidly transmitted among people, the mortality rate reached 2% early in the pandemic and the most severe cases were found in immunocompromised patients and patients with underlying conditions 6 …”

Section: Introductionmentioning

confidence: 99%

SARS‐CoV‐2 infection of polarized human airway epithelium induces necroptosis that causes airway epithelial barrier dysfunction

Hao,

Ning,

Kuz

et al. 2023

Journal of Medical Virology

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Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) is the cause the ongoing pandemic of coronavirus disease 2019 (COVID19). One key feature associated with COVID‐19 is excessive pro‐inflammatory cytokine production that leads to severe acute respiratory distress syndrome. Although the cytokine storm induces inflammatory cell death in the host, which type of programmed cell death mechanism that occurs in various organs and cells remains elusive. Using an in vitro culture model of polarized human airway epithelium (HAE), we observed that necroptosis, but not apoptosis or pyroptosis, plays an essential role in the damage of the epithelial barrier of polarized HAE infected with SARS‐CoV‐2. Pharmacological inhibitors of necroptosis, necrostatin‐2 and necrosulfonamide, efficiently prevented cell death and epithelial barrier dysfunction caused by SARS‐CoV‐2 infection. Moreover, the silencing of genes that are involved in necroptosis, RIPK1, RIPK3, and MLKL, ameliorated airway epithelial damage of the polarized HAE infected with SARS‐CoV‐2. This study, for the first time, confirms that SARS‐CoV‐2 infection triggers necroptosis that disrupts the barrier function of human airway epithelia in vitro.

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Section: Introductionmentioning

confidence: 99%

SARS‐CoV‐2 infection of polarized human airway epithelium induces necroptosis that causes airway epithelial barrier dysfunction

Hao,

Ning,

Kuz

et al. 2023

Journal of Medical Virology

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“…From 2020 to 2022, some epidemiological models were developed to describe the betweenhost transmission of COVID-19 co-infection with other diseases such as bacteria/COVID-19 [46], tuberculosis/COVID-19 [47], Dengue/COVID-19 [48], Dengue/HIV/COVID-19 [49], ZIKV/COVID-19 [50], HIV/COVID-19 [51], and influenza/COVID-19 [52]. On the other hand, virological models that describe the in-host dynamics of SARS-CoV-2 with coinfection with other micro-organisms have been investigated in recent studies: influenza A virus/SARS-CoV-2 [53,54], malaria/SARS-CoV-2 [55], HIV/SARS-CoV-2 [56], and bacteria/ SARS-CoV-2 [57].…”

Section: Htlv-i and Sars-cov-2 Co-infection Modelmentioning

confidence: 99%

Global Dynamics of an HTLV-I and SARS-CoV-2 Co-Infection Model with Diffusion

et al. 2023

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel respiratory virus that causes coronavirus disease 2019 (COVID-19). Symptoms of COVID-19 range from mild to severe illness. It was observed that disease progression in COVID-19 patients depends on their immune response, especially in elderly patients whose immune system suppression may put them at increased risk of infection. Human T-cell lymphotropic virus type-I (HTLV-I) attacks the CD4+ T cells (T cells) of the immune system and leads to immune dysfunction. Co-infection with HTLV-I and SARS-CoV-2 has been reported in recent studies. Modeling HTLV-I and SARS-CoV-2 co-infection can be a helpful tool to understand the in-host co-dynamics of these viruses. The aim of this study was to construct a model that characterizes the in-host dynamics of HTLV-I and SARS-CoV-2 co-infection. By considering the mobility of the viruses and cells, the model is represented by a system of partial differential equations (PDEs). The system contains two independent variables, time t and position x, and seven dependent variables for representing the densities of healthy epithelial cells (ECs), latent SARS-CoV-2-infected ECs, active SARS-CoV-2-infected ECs, SARS-CoV-2, healthy T cells, latent HTLV-I-infected T cells and active HTLV-I-infected T cells. We first studied the fundamental properties of the solutions of the system, then deduced all steady states and proved their global properties. We examined the global stability of the steady states by constructing appropriate Lyapunov functions. The analytical results were illustrated by performing numerical simulations. We discussed the effect of HTLV-I infection on COVID-19 progression. The results suggest that patients with HTLV-I have a weakened immune response; consequently, their risk of COVID-19 infection may be increased.

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“…Mathematical models to study the co-interactions between SARS-CoV-2 infection and other diseases have attracted the attention of several researchers [22] , [23] , [24] , [25] , [26] , [27] , [28] , [29] , [30] , [31] , [32] , [33] . The authors in [22] analyzed a co-dynamical model for dengue and COVID-19, comparing model solutions using various fractional operators.…”

Section: Introductionmentioning

confidence: 99%