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Mathematical Model of SAR-CoV-2 and Influenza A Virus Coinfection within Host with CTL-Mediated Immunity

Jambura Journal of Biomathematics (JJBM) · Vol. ume (2024) · hlm. 95–108

DOI
10.37905/jjbm.v5i2.27782
ISSN
2723-0317
Terbit
2024-12-31
Penerbit
Department of Mathematics, Universitas Negeri Gorontalo
Bahasa
eng
Lisensi
creativecommons.org/licenses/by-nc/4.0

Abstrak

Coinfection of SARS-CoV-2 and Influenza A virus within a host poses a unique challenge in understanding immunological dynamics, especially the role of cytotoxic T lymphocytes (CTL) in mediating the immune response. This work present a mathematical model to examine the dynamics of coinfection within a host, highlighting CTL-mediated immunity. Generally, this model encompasses several compartments, including epithelial cells, free viruses, and CTLs specific of both SARS-CoV-2 and Influenza A. The basic properties of the model, equilibrum state analysis, stability using the Lyapunov function, and numerical simulations are examined to investigate the dynamics behavior of the model. Eight equilibrium states are identified: the virus-free equilibrium (E0), single SARS-CoV-2 infection without CTLs (E1), single Influenza A virus infection without CTLs (E2), single SARS-CoV-2 infection with SARS-CoV-2-specific CTLs (E3), single Influenza A virus infection with Influenza A virus-specific CTLs (E4), SARS-CoV-2 and Influenza A virus coinfection with SARS-CoV-2-specific CTLs (E5), SARS-CoV-2 and Influenza A virus coinfection with Influenza A virus-specific CTLs (E6), and SARS-CoV-2 and Influenza A virus coinfection with both SARS-CoV-2-specific and Influenza A virus-specific CTLs (E7). The existence and stability regions for each equilibrium state are determined and represented in the R1-R2 plane as threshold functions within the model. Numerical simulations confirm the results of the qualitative analysis, demonstrating that CTLs specific to SARS-CoV-2 and Influenza A virus can be activated, reducing the number of infected epithelial cells as well as inhibiting virus transmission within epithelial cells. Furthermore, analysis of parameter changes shows that increasing the proliferation rate of epithelial cells and CTLs, while lowering the virus formation rate, can shift the system's stability threshold and stabilize it at the virus-free equilibrium.

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  • Sumatera Institute of Technology
  • Sunan Gunung Djati State Islamic University Bandung
  • Bandung Institute of Technology
  • Padjadjaran University
  • Korea Institute of Ocean Science and Technology
  • Institut Teknologi Statistika dan Bisnis Muhammadiyah Semarang
  • Politeknik Negeri Padang
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Rekan penulisOrganisasiArtikel bersama
Dear Michiko Mutiara NoorSumatera Institute of Technology3
Tiara Shofi EdrianiSumatera Institute of Technology2
Edy SoewonoBandung Institute of Technology2
Eristia ArfiSumatera Institute of Technology1
Dwi Mutiara PutriSumatera Institute of Technology1
Yeni Gede WibaraniSumatera Institute of Technology1
Nurul Indah SafitriSumatera Institute of Technology1
Suli Windi AstutiSumatera Institute of Technology1
M. Diwa Sandika AditamaSumatera Institute of Technology1
Fadilah IlahiSunan Gunung Djati State Islamic University Bandung1
Della Isna AmatillahSunan Gunung Djati State Islamic University Bandung1
Faizal Ade Rahmahuddin AbdullahKorea Institute of Ocean Science and Technology1
Diny ZulkarnaenSunan Gunung Djati State Islamic University Bandung1
Ichwal Afrizan ShiddiqieSunan Gunung Djati State Islamic University Bandung1
Arista Fitri DianaInstitut Teknologi Statistika dan Bisnis Muhammadiyah Semarang1
Asep Solih AwalluddinSunan Gunung Djati State Islamic University Bandung1
Hathifah Fidya AmaliaSunan Gunung Djati State Islamic University Bandung1
Inge WahyuniAfiliasi tidak diketahui1
David Eka PutraPoliteknik Negeri Padang1
Halim MudiaAfiliasi tidak diketahui1
Nuning NurainiBandung Institute of Technology1
Nursanti AnggrianiPadjadjaran University1
Asep Kuswandi SupriatnaPadjadjaran University1
Laura LauraPadjadjaran University1
Zunanik MufidahSumatera Institute of Technology1
Sri HaryaniState University of Semarang1
Utriweni MukhaiyarBandung Institute of Technology1
Riani UtamiBandung Institute of Technology1
Rifky FauziSumatera Institute of Technology1
Gres MarettaSumatera Institute of Technology1
Saefudin SaefudinAfiliasi tidak diketahui1
Amalia StyaningrumAfiliasi tidak diketahui1
Rifky FauziSumatera Institute of Technology1
SH Yoga AndriyantoSumatera Institute of Technology1
Aswan Anggun PribadiSumatera Institute of Technology1
Ciptaning Weargo JatiLampung University1

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Sumber metadata: OAI-PMH (metadata jurnal) http://ejurnal.ung.ac.id/index.php/JJBM/oai, pertama di-harvest 9 Nov 2026, terakhir terlihat 9 Nov 2026.
Metadata asli (oai_dc) 
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	<dc:title xml:lang="en-US">Mathematical Model of SAR-CoV-2 and Influenza A Virus Coinfection within Host with CTL-Mediated Immunity</dc:title>
	<dc:creator>Khumaeroh, Mia Siti</dc:creator>
	<dc:creator>Nuwari, Najmudin</dc:creator>
	<dc:creator>Erianto, Elvi Syukrina</dc:creator>
	<dc:creator>Rizka, Nela</dc:creator>
	<dc:subject xml:lang="en-US">SARS-CoV-2;  Influenza A virus; Coinfection; CTL; Lyapunov</dc:subject>
	<dc:description xml:lang="en-US">Coinfection of SARS-CoV-2 and Influenza A virus within a host poses a unique challenge in understanding immunological dynamics, especially the role of cytotoxic T lymphocytes (CTL) in mediating the immune response. This work present a mathematical model to examine the dynamics of coinfection within a host, highlighting CTL-mediated immunity. Generally, this model encompasses several compartments, including epithelial cells, free viruses, and CTLs specific of both SARS-CoV-2 and Influenza A. The basic properties of the model, equilibrum state analysis, stability using the Lyapunov function, and numerical simulations are examined to investigate the dynamics behavior of the model. Eight equilibrium states are identified: the virus-free equilibrium (E0), single SARS-CoV-2 infection without CTLs (E1), single Influenza A virus infection without CTLs (E2), single SARS-CoV-2 infection with SARS-CoV-2-specific CTLs (E3), single Influenza A virus infection with Influenza A virus-specific CTLs (E4), SARS-CoV-2 and Influenza A virus coinfection with SARS-CoV-2-specific CTLs (E5), SARS-CoV-2 and Influenza A virus coinfection with Influenza A virus-specific CTLs (E6), and SARS-CoV-2 and Influenza A virus coinfection with both SARS-CoV-2-specific and Influenza A virus-specific CTLs (E7). The existence and stability regions for each equilibrium state are determined and represented in the R1-R2 plane as threshold functions within the model. Numerical simulations confirm the results of the qualitative analysis, demonstrating that CTLs specific to SARS-CoV-2 and Influenza A virus can be activated, reducing the number of infected epithelial cells as well as inhibiting virus transmission within epithelial cells. Furthermore, analysis of parameter changes shows that increasing the proliferation rate of epithelial cells and CTLs, while lowering the virus formation rate, can shift the system's stability threshold and stabilize it at the virus-free equilibrium.</dc:description>
	<dc:publisher xml:lang="en-US">Department of Mathematics, Universitas Negeri Gorontalo</dc:publisher>
	<dc:contributor xml:lang="en-US"></dc:contributor>
	<dc:date>2024-12-31</dc:date>
	<dc:type>info:eu-repo/semantics/article</dc:type>
	<dc:type>info:eu-repo/semantics/publishedVersion</dc:type>
	<dc:type xml:lang="en-US">Peer-reviewed Article</dc:type>
	<dc:format>application/pdf</dc:format>
	<dc:identifier>https://ejurnal.ung.ac.id/index.php/JJBM/article/view/27782</dc:identifier>
	<dc:identifier>10.37905/jjbm.v5i2.27782</dc:identifier>
	<dc:source xml:lang="en-US">Jambura Journal of Biomathematics (JJBM); Volume 5, Issue 2: December 2024; 95-108</dc:source>
	<dc:source>2723-0317</dc:source>
	<dc:source>10.37905/jjbm.v5i2</dc:source>
	<dc:language>eng</dc:language>
	<dc:relation>https://ejurnal.ung.ac.id/index.php/JJBM/article/view/27782/9862</dc:relation>
	<dc:rights xml:lang="en-US">Copyright (c) 2024 Mia Siti Khumaeroh, Najmudin Nuwari, Elvi Syukrina Erianto, Nela Rizka</dc:rights>
	<dc:rights xml:lang="en-US">https://creativecommons.org/licenses/by-nc/4.0</dc:rights>
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