Differential effects of CMV infection on the viability of cardiac cells
Abstract Cytomegalovirus (CMV) is a widely prevalent herpesvirus that reaches seroprevalence rates of up to 95% in several parts of the world. The majority of CMV infections are asymptomatic, albeit they have severe detrimental effects on immunocompromised individuals. Congenital CMV infection is a...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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Nature Publishing Group
2023-04-01
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| Series: | Cell Death Discovery |
| Online Access: | https://doi.org/10.1038/s41420-023-01408-y |
| _version_ | 1797850159467462656 |
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| author | Santosh K. Yadav Flobater I. Gawargi Mohammad H. Hasan Ritesh Tandon Jason W. Upton Paras K. Mishra |
| author_facet | Santosh K. Yadav Flobater I. Gawargi Mohammad H. Hasan Ritesh Tandon Jason W. Upton Paras K. Mishra |
| author_sort | Santosh K. Yadav |
| collection | DOAJ |
| description | Abstract Cytomegalovirus (CMV) is a widely prevalent herpesvirus that reaches seroprevalence rates of up to 95% in several parts of the world. The majority of CMV infections are asymptomatic, albeit they have severe detrimental effects on immunocompromised individuals. Congenital CMV infection is a leading cause of developmental abnormalities in the USA. CMV infection is a significant risk factor for cardiovascular diseases in individuals of all ages. Like other herpesviruses, CMV regulates cell death for its replication and establishes and maintains a latent state in the host. Although CMV-mediated regulation of cell death is reported by several groups, it is unknown how CMV infection affects necroptosis and apoptosis in cardiac cells. Here, we infected primary cardiomyocytes, the contractile cells in the heart, and primary cardiac fibroblasts with wild-type and cell-death suppressor deficient mutant CMVs to determine how CMV regulates necroptosis and apoptosis in cardiac cells. Our results reveal that CMV infection prevents TNF-induced necroptosis in cardiomyocytes; however, the opposite phenotype is observed in cardiac fibroblasts. CMV infection also suppresses inflammation, reactive oxygen species (ROS) generation, and apoptosis in cardiomyocytes. Furthermore, CMV infection improves mitochondrial biogenesis and viability in cardiomyocytes. We conclude that CMV infection differentially affects the viability of cardiac cells. |
| first_indexed | 2024-04-09T18:56:59Z |
| format | Article |
| id | doaj.art-4c062d611b2e4c5fa9061e4a297584b7 |
| institution | Directory Open Access Journal |
| issn | 2058-7716 |
| language | English |
| last_indexed | 2024-04-09T18:56:59Z |
| publishDate | 2023-04-01 |
| publisher | Nature Publishing Group |
| record_format | Article |
| series | Cell Death Discovery |
| spelling | doaj.art-4c062d611b2e4c5fa9061e4a297584b72023-04-09T11:08:09ZengNature Publishing GroupCell Death Discovery2058-77162023-04-01911910.1038/s41420-023-01408-yDifferential effects of CMV infection on the viability of cardiac cellsSantosh K. Yadav0Flobater I. Gawargi1Mohammad H. Hasan2Ritesh Tandon3Jason W. Upton4Paras K. Mishra5Department of Cellular and Integrative Physiology, University of Nebraska Medical CenterDepartment of Cellular and Integrative Physiology, University of Nebraska Medical CenterDepartment of Cell and Molecular Biology, Center for Immunology and Microbial Research, University of Mississippi Medical CenterDepartment of Cell and Molecular Biology, Center for Immunology and Microbial Research, University of Mississippi Medical CenterDepartment of Biological Sciences, Auburn UniversityDepartment of Cellular and Integrative Physiology, University of Nebraska Medical CenterAbstract Cytomegalovirus (CMV) is a widely prevalent herpesvirus that reaches seroprevalence rates of up to 95% in several parts of the world. The majority of CMV infections are asymptomatic, albeit they have severe detrimental effects on immunocompromised individuals. Congenital CMV infection is a leading cause of developmental abnormalities in the USA. CMV infection is a significant risk factor for cardiovascular diseases in individuals of all ages. Like other herpesviruses, CMV regulates cell death for its replication and establishes and maintains a latent state in the host. Although CMV-mediated regulation of cell death is reported by several groups, it is unknown how CMV infection affects necroptosis and apoptosis in cardiac cells. Here, we infected primary cardiomyocytes, the contractile cells in the heart, and primary cardiac fibroblasts with wild-type and cell-death suppressor deficient mutant CMVs to determine how CMV regulates necroptosis and apoptosis in cardiac cells. Our results reveal that CMV infection prevents TNF-induced necroptosis in cardiomyocytes; however, the opposite phenotype is observed in cardiac fibroblasts. CMV infection also suppresses inflammation, reactive oxygen species (ROS) generation, and apoptosis in cardiomyocytes. Furthermore, CMV infection improves mitochondrial biogenesis and viability in cardiomyocytes. We conclude that CMV infection differentially affects the viability of cardiac cells.https://doi.org/10.1038/s41420-023-01408-y |
| spellingShingle | Santosh K. Yadav Flobater I. Gawargi Mohammad H. Hasan Ritesh Tandon Jason W. Upton Paras K. Mishra Differential effects of CMV infection on the viability of cardiac cells Cell Death Discovery |
| title | Differential effects of CMV infection on the viability of cardiac cells |
| title_full | Differential effects of CMV infection on the viability of cardiac cells |
| title_fullStr | Differential effects of CMV infection on the viability of cardiac cells |
| title_full_unstemmed | Differential effects of CMV infection on the viability of cardiac cells |
| title_short | Differential effects of CMV infection on the viability of cardiac cells |
| title_sort | differential effects of cmv infection on the viability of cardiac cells |
| url | https://doi.org/10.1038/s41420-023-01408-y |
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