A Coupled Model of the Cardiovascular and Immune Systems to Analyze the Effects of COVID-19 Infection
The COVID-19 pandemic has underscored the importance of understanding the interplay between the cardiovascular and immune systems during viral infections. SARS-CoV-2 enters human cells via the ACE-2 enzyme, initiating a cascade of immune responses. This study presents a coupled mathematical model th...
Saved in:
| Main Authors: | , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2025-03-01
|
| Series: | BioTech |
| Subjects: | |
| Online Access: | https://www.mdpi.com/2673-6284/14/1/19 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1849341887834488832 |
|---|---|
| author | Camila Ribeiro Passos Alexandre Altamir Moreira Ruy Freitas Reis Rodrigo Weber dos Santos Marcelo Lobosco Bernardo Martins Rocha |
| author_facet | Camila Ribeiro Passos Alexandre Altamir Moreira Ruy Freitas Reis Rodrigo Weber dos Santos Marcelo Lobosco Bernardo Martins Rocha |
| author_sort | Camila Ribeiro Passos |
| collection | DOAJ |
| description | The COVID-19 pandemic has underscored the importance of understanding the interplay between the cardiovascular and immune systems during viral infections. SARS-CoV-2 enters human cells via the ACE-2 enzyme, initiating a cascade of immune responses. This study presents a coupled mathematical model that integrates the cardiovascular system (CVS) and immune system (IS), capturing their complex interactions during infection. The CVS model, based on ordinary differential equations, describes heart dynamics and pulmonary and systemic circulation, while the IS model simulates immune responses to SARS-CoV-2, including immune cell interactions and cytokine production. A coupling strategy transfers information from the IS to the CVS at specific intervals, enabling the exploration of immune-driven cardiovascular effects. Numerical simulations examined how these interactions influence infection severity and recovery. The coupled model accurately replicated the evolution of cardiac function in survivors and non-survivors of COVID-19. Survivors exhibited a left ventricular ejection fraction (LVEF) reduction of up to <inline-formula><math xmlns="http://www.w3.org/1998/Math/MathML" display="inline"><semantics><mrow><mn>25</mn><mo>%</mo></mrow></semantics></math></inline-formula> while remaining within normal limits, whereas non-survivors showed a severe 4-fold decline, indicative of myocardial dysfunction. Similarly, the right ventricular ejection fraction (RV EF) decreased by approximately <inline-formula><math xmlns="http://www.w3.org/1998/Math/MathML" display="inline"><semantics><mrow><mn>50</mn><mo>%</mo></mrow></semantics></math></inline-formula> in survivors but underwent a drastic 5-fold reduction in non-survivors. These findings highlight the model’s capacity to distinguish differential cardiac dysfunction across clinical outcomes and its potential to enhance our understanding of COVID-19 pathophysiology. |
| format | Article |
| id | doaj-art-1d0ce99f4fe74becbc308bd74421f277 |
| institution | Kabale University |
| issn | 2673-6284 |
| language | English |
| publishDate | 2025-03-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | BioTech |
| spelling | doaj-art-1d0ce99f4fe74becbc308bd74421f2772025-08-20T03:43:33ZengMDPI AGBioTech2673-62842025-03-011411910.3390/biotech14010019A Coupled Model of the Cardiovascular and Immune Systems to Analyze the Effects of COVID-19 InfectionCamila Ribeiro Passos0Alexandre Altamir Moreira1Ruy Freitas Reis2Rodrigo Weber dos Santos3Marcelo Lobosco4Bernardo Martins Rocha5Computational Engineering, Federal University of Juiz de Fora, Juiz de Fora 36036-900, BrazilMechanical Engineering, Federal University of Juiz de Fora, Juiz de Fora 36036-900, BrazilGraduate Program in Computational Modeling, Federal University of Juiz de Fora, Juiz de Fora 36036-900, BrazilGraduate Program in Computational Modeling, Federal University of Juiz de Fora, Juiz de Fora 36036-900, BrazilGraduate Program in Computational Modeling, Federal University of Juiz de Fora, Juiz de Fora 36036-900, BrazilGraduate Program in Computational Modeling, Federal University of Juiz de Fora, Juiz de Fora 36036-900, BrazilThe COVID-19 pandemic has underscored the importance of understanding the interplay between the cardiovascular and immune systems during viral infections. SARS-CoV-2 enters human cells via the ACE-2 enzyme, initiating a cascade of immune responses. This study presents a coupled mathematical model that integrates the cardiovascular system (CVS) and immune system (IS), capturing their complex interactions during infection. The CVS model, based on ordinary differential equations, describes heart dynamics and pulmonary and systemic circulation, while the IS model simulates immune responses to SARS-CoV-2, including immune cell interactions and cytokine production. A coupling strategy transfers information from the IS to the CVS at specific intervals, enabling the exploration of immune-driven cardiovascular effects. Numerical simulations examined how these interactions influence infection severity and recovery. The coupled model accurately replicated the evolution of cardiac function in survivors and non-survivors of COVID-19. Survivors exhibited a left ventricular ejection fraction (LVEF) reduction of up to <inline-formula><math xmlns="http://www.w3.org/1998/Math/MathML" display="inline"><semantics><mrow><mn>25</mn><mo>%</mo></mrow></semantics></math></inline-formula> while remaining within normal limits, whereas non-survivors showed a severe 4-fold decline, indicative of myocardial dysfunction. Similarly, the right ventricular ejection fraction (RV EF) decreased by approximately <inline-formula><math xmlns="http://www.w3.org/1998/Math/MathML" display="inline"><semantics><mrow><mn>50</mn><mo>%</mo></mrow></semantics></math></inline-formula> in survivors but underwent a drastic 5-fold reduction in non-survivors. These findings highlight the model’s capacity to distinguish differential cardiac dysfunction across clinical outcomes and its potential to enhance our understanding of COVID-19 pathophysiology.https://www.mdpi.com/2673-6284/14/1/19COVID-19viral infectioncardiovascular systemimmune systemmathematical models |
| spellingShingle | Camila Ribeiro Passos Alexandre Altamir Moreira Ruy Freitas Reis Rodrigo Weber dos Santos Marcelo Lobosco Bernardo Martins Rocha A Coupled Model of the Cardiovascular and Immune Systems to Analyze the Effects of COVID-19 Infection BioTech COVID-19 viral infection cardiovascular system immune system mathematical models |
| title | A Coupled Model of the Cardiovascular and Immune Systems to Analyze the Effects of COVID-19 Infection |
| title_full | A Coupled Model of the Cardiovascular and Immune Systems to Analyze the Effects of COVID-19 Infection |
| title_fullStr | A Coupled Model of the Cardiovascular and Immune Systems to Analyze the Effects of COVID-19 Infection |
| title_full_unstemmed | A Coupled Model of the Cardiovascular and Immune Systems to Analyze the Effects of COVID-19 Infection |
| title_short | A Coupled Model of the Cardiovascular and Immune Systems to Analyze the Effects of COVID-19 Infection |
| title_sort | coupled model of the cardiovascular and immune systems to analyze the effects of covid 19 infection |
| topic | COVID-19 viral infection cardiovascular system immune system mathematical models |
| url | https://www.mdpi.com/2673-6284/14/1/19 |
| work_keys_str_mv | AT camilaribeiropassos acoupledmodelofthecardiovascularandimmunesystemstoanalyzetheeffectsofcovid19infection AT alexandrealtamirmoreira acoupledmodelofthecardiovascularandimmunesystemstoanalyzetheeffectsofcovid19infection AT ruyfreitasreis acoupledmodelofthecardiovascularandimmunesystemstoanalyzetheeffectsofcovid19infection AT rodrigoweberdossantos acoupledmodelofthecardiovascularandimmunesystemstoanalyzetheeffectsofcovid19infection AT marcelolobosco acoupledmodelofthecardiovascularandimmunesystemstoanalyzetheeffectsofcovid19infection AT bernardomartinsrocha acoupledmodelofthecardiovascularandimmunesystemstoanalyzetheeffectsofcovid19infection AT camilaribeiropassos coupledmodelofthecardiovascularandimmunesystemstoanalyzetheeffectsofcovid19infection AT alexandrealtamirmoreira coupledmodelofthecardiovascularandimmunesystemstoanalyzetheeffectsofcovid19infection AT ruyfreitasreis coupledmodelofthecardiovascularandimmunesystemstoanalyzetheeffectsofcovid19infection AT rodrigoweberdossantos coupledmodelofthecardiovascularandimmunesystemstoanalyzetheeffectsofcovid19infection AT marcelolobosco coupledmodelofthecardiovascularandimmunesystemstoanalyzetheeffectsofcovid19infection AT bernardomartinsrocha coupledmodelofthecardiovascularandimmunesystemstoanalyzetheeffectsofcovid19infection |