Cytomegalovirus Latency Fuels Inflammation Following Myocardial Infarction
Abstract
BACKGROUND: Epidemiological studies have consistently associated cytomegalovirus (CMV) seropositivity with adverse cardiovascular outcomes. However, the mechanisms by which cytomegalovirus infection impacts pathophysiology in the heart remain poorly understood. In this study, we sought to dissect how latent murine cytomegalovirus infection impacts cardiac immune cell dynamics at steady-state and during postmyocardial infarction (MI) repair. METHODS: Experimental MI studies were conducted in C57BL/6J mice previously infected with murine cytomegalovirus. In situ inflammatory responses were characterized by spectral flow cytometry, bulk and single-cell RNA/T-cell receptor (TCR) sequencing, whereas cardiac function was monitored by echocardiography and cardiac magnetic resonance imaging. Moreover, we retrospectively assessed the cytomegalovirus serostatus and associated T-cell expansions in a well-characterized patient cohort with longitudinal cardiac magnetic resonance imaging data available and performed bulk TCR sequencing on peripheral blood and myocardial samples to identify cytomegalovirus-specific TCRs. RESULTS: Our findings show that exposure to murine cytomegalovirus induces long-term changes in the cardiac transcriptional profile and alterations in various cardiac-resident immune cell populations, including the establishment of virus-specific memory CD8 + T-cell residency. Compared with infarcted controls, mice previously exposed to murine cytomegalovirus exhibited stronger inflammatory responses marked by increased CD8 + T-cell infiltration and worsened cardiac function following MI. These observations in mice were supported by data from patients with cytomegalovirus seropositive MI, who harbored cytomegalovirus-responsive T cells in the heart. CONCLUSIONS: Our findings demonstrate that latent cytomegalovirus infection leads to long-term changes in the cardiac microenvironment, which ultimately impair post-MI healing outcomes.
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BibTeX
@article{dapergola2026cytomegalovirus,
title = {{Cytomegalovirus Latency Fuels Inflammation Following Myocardial Infarction}},
author = {Eleni Dapergola and Marko Šustić and Diyaaeldin Ashour and Ebram Tharwat Melika and Maja Cokarić Brdovčak and Jelena Materljan Franki and Mijo Golemac and Berislav Lisnić and Ema Bellulovich and Valérie Boivin-Jahns and Tobias Krammer and Kenz Le Gouge and Lavinia Rech and Verena Stangl and Karl Kashofer and Peter Rainer and Roland Jahns and Encarnita Mariotti-Ferrandiz and Hamid Marwan and Maxim Terekhov and Mohammadreza Keshtkar and Antoine-Emmanuel Saliba and Clement Cochain and Panagiota Arampatzi and Mugdha Srivastava and Sven Plein and Yasemin Ekinci and Ioakim Spyridopoulos and Stipan Jonjić and Ulrich Hofmann and Stefan Frantz and Ilija Brizić and Georg Gasteiger and Gustavo Campos Ramos},
journal = {Circulation Research},
year = {2026},
month = sep,
doi = {10.1161/circresaha.125.327799},
url = {https://hal.science/hal-05780552v1},
note = {CC BY},
}
RIS
TY - JOUR
TI - Cytomegalovirus Latency Fuels Inflammation Following Myocardial Infarction
AU - Eleni Dapergola
AU - Marko Šustić
AU - Diyaaeldin Ashour
AU - Ebram Tharwat Melika
AU - Maja Cokarić Brdovčak
AU - Jelena Materljan Franki
AU - Mijo Golemac
AU - Berislav Lisnić
AU - Ema Bellulovich
AU - Valérie Boivin-Jahns
AU - Tobias Krammer
AU - Kenz Le Gouge
AU - Lavinia Rech
AU - Verena Stangl
AU - Karl Kashofer
AU - Peter Rainer
AU - Roland Jahns
AU - Encarnita Mariotti-Ferrandiz
AU - Hamid Marwan
AU - Maxim Terekhov
AU - Mohammadreza Keshtkar
AU - Antoine-Emmanuel Saliba
AU - Clement Cochain
AU - Panagiota Arampatzi
AU - Mugdha Srivastava
AU - Sven Plein
AU - Yasemin Ekinci
AU - Ioakim Spyridopoulos
AU - Stipan Jonjić
AU - Ulrich Hofmann
AU - Stefan Frantz
AU - Ilija Brizić
AU - Georg Gasteiger
AU - Gustavo Campos Ramos
PY - 2026
DA - 2026/09/14
JO - Circulation Research
DO - 10.1161/circresaha.125.327799
UR - https://hal.science/hal-05780552v1
AB - BACKGROUND: Epidemiological studies have consistently associated cytomegalovirus (CMV) seropositivity with adverse cardiovascular outcomes. However, the mechanisms by which cytomegalovirus infection impacts pathophysiology in the heart remain poorly understood. In this study, we sought to dissect how latent murine cytomegalovirus infection impacts cardiac immune cell dynamics at steady-state and during postmyocardial infarction (MI) repair. METHODS: Experimental MI studies were conducted in C57BL/6J mice previously infected with murine cytomegalovirus. In situ inflammatory responses were characterized by spectral flow cytometry, bulk and single-cell RNA/T-cell receptor (TCR) sequencing, whereas cardiac function was monitored by echocardiography and cardiac magnetic resonance imaging. Moreover, we retrospectively assessed the cytomegalovirus serostatus and associated T-cell expansions in a well-characterized patient cohort with longitudinal cardiac magnetic resonance imaging data available and performed bulk TCR sequencing on peripheral blood and myocardial samples to identify cytomegalovirus-specific TCRs. RESULTS: Our findings show that exposure to murine cytomegalovirus induces long-term changes in the cardiac transcriptional profile and alterations in various cardiac-resident immune cell populations, including the establishment of virus-specific memory CD8 + T-cell residency. Compared with infarcted controls, mice previously exposed to murine cytomegalovirus exhibited stronger inflammatory responses marked by increased CD8 + T-cell infiltration and worsened cardiac function following MI. These observations in mice were supported by data from patients with cytomegalovirus seropositive MI, who harbored cytomegalovirus-responsive T cells in the heart. CONCLUSIONS: Our findings demonstrate that latent cytomegalovirus infection leads to long-term changes in the cardiac microenvironment, which ultimately impair post-MI healing outcomes.
SN - 0009-7330
SN - 1524-4571
ER -