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Viruses
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Virus-Induced Myocarditis
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Virus-Induced Myocarditis

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Human Virology and Viral Diseases".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 18659

Special Issue Editors

Prof. Dr. Antje Beling

E-Mail Website
Guest Editor
1. Charité—Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health (BIH), Institute of Biochemistry, Berlin, Germany
2. Deutsches Zentrum für Herz-Kreislauf-Forschung (DZHK), partner side Berlin, Germany
Interests: ISG15/ISGylation with a focus on host-pathogen interactions;enterovirus infection biology;ubiquitin-proteasome system;immunopathology with a focus on cardiac inflammation;immunometabolism;immuno-cardio-oncology
Prof. Dr. Karin Klingel

E-Mail Website
Guest Editor
Cardiopathology, Institute for Pathology and Neuropathology, University Hospital Tuebingen, Tuebingen, Germany
Interests: hepatitis viruses; influenza viruses; human papillomaviruses; COVID-19
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Myocarditis is a condition resulting from inflammation of the heart muscle which, in developed countries, most commonly results from a virus infection and has most severe course in childhood and adolescence. As a first line of defense, virus-infected cells in the heart produce type I interferons (IFNs), which are known to orchestrate a complex defense network within infected cells, but also in nearby cells. The IFN signature, triggered by virus infection of heart muscle cells, might be highly variable for several viruses. Consistent with the fact that a unique set of ISGs targets distinct viruses, a specific ISG signature renders protection of the host for defined pathogens and, on the other hand, might have less pronounced effect for others. It is less clear to what extent congenital aspects of the host that control ISG signatures can influence susceptibility to viral myocarditis.

In this Special Issue, we discuss how viruses with known affection of cardiac cells affect host defense systems, defining the underlying molecular mechanisms of host–pathogen interactions, the physiological relevance of innate immune defense pathways and the translational potential of inhibition or activation of these pathways. We will also discuss strategies how viruses have evolved to escape innate host defense strategies.

Prof. Dr. Antje Beling
Prof. Dr. Karin Klingel
Guest Editors

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Keywords

  • virus
  • myocarditis
  • innate immune response
  • type I interferon
  • host–pathogen interaction
  • immune escape mechanism

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Published Papers (5 papers)

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Research

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15 pages, 2957 KiB  
Article
The Spontaneous Course of Human Herpesvirus 6 DNA-Associated Myocarditis and the Effect of Immunosuppressive Intervention
by Ahmed Elsanhoury, Uwe Kühl, Bruno Stautner, Oliver Klein, Alexander Krannich, Daniel Morris, Monika Willner, Ewa Jankowska, Karin Klingel, Sophie Van Linthout and Carsten Tschöpe
Viruses 2022, 14(2), 299; https://doi.org/10.3390/v14020299 - 31 Jan 2022
Cited by 16 | Viewed by 3801
Abstract
Introduction: This study investigated the spontaneous clinical course of patients with endomyocardial biopsy (EMB)-proven lymphocytic myocarditis and cardiac human herpesvirus 6 (HHV6) DNA presence, and the effectiveness of steroid-based intervention in HHV6-positive patients. Results: 756 heart failure (HF) patients underwent an EMB procedure [...] Read more.
Introduction: This study investigated the spontaneous clinical course of patients with endomyocardial biopsy (EMB)-proven lymphocytic myocarditis and cardiac human herpesvirus 6 (HHV6) DNA presence, and the effectiveness of steroid-based intervention in HHV6-positive patients. Results: 756 heart failure (HF) patients underwent an EMB procedure to determine the underlying cause of unexplained HF. Low levels of HHV6 DNA, detectable by nested PCR only, were found in 10.4% of the cases (n = 79) of which 62% (n = 49) showed myocardial inflammation. The spontaneous course of patients with EMB-proven HHV6 DNA-associated lymphocytic myocarditis (n = 26) showed significant improvements in the left ventricular ejection fraction (LVEF) and clinical symptoms, respectively, in 15/26 (60%) patients, 3–12 months after disease onset. EMB mRNA expression of components of the NLRP3 inflammasome pathway and protein analysis of cardiac remodeling markers, analyzed by real-time PCR and MALDI mass spectrometry, respectively, did not differ between HHV6-positive and -negative patients. In another cohort of patients with ongoing symptoms related to lymphocytic myocarditis associated with cardiac levels of HHV6-DNA copy numbers <500 copies/µg cardiac DNA, quantified by real-time PCR, the efficacy and safety of steroid-based immunosuppression for six months was investigated. Steroid-based immunosuppression improved the LVEF (≥5%) in 8/10 patients and reduced cardiac inflammation in 7/10 patients, without an increase in cardiac HHV6 DNA levels in follow-up EMBs. Conclusion: Low HHV6 DNA levels are frequently detected in the myocardium, independent of inflammation. In patients with lymphocytic myocarditis with low levels of HHV6 DNA, the spontaneous clinical improvement is nearby 60%. In selected symptomatic patients with cardiac HHV6 DNA copy numbers less than 500 copies/µg cardiac DNA and without signs of an active systemic HHV6 infection, steroid-based therapy was found to be effective and safe. This finding needs to be further confirmed in large, randomized trials. Full article
(This article belongs to the Special Issue Virus-Induced Myocarditis)
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17 pages, 2959 KiB  
Article
In Vitro Model Systems of Coxsackievirus B3-Induced Myocarditis: Comparison of Commonly Used Cell Lines and Characterization of CVB3-Infected iCell® Cardiomyocytes
by Lisa Kraft, Martina Sauter, Guiscard Seebohm and Karin Klingel
Viruses 2021, 13(9), 1835; https://doi.org/10.3390/v13091835 - 14 Sep 2021
Cited by 9 | Viewed by 3475
Abstract
Coxsackievirus B3 (CVB3) belongs to the enteroviruses, which are a well-known cause of acute and chronic myocarditis, primarily infecting cardiac myocytes. As primary human cardiomyocytes are difficult to obtain, viral myocarditis is quite frequently studied in vitro in different non-cardiac and cardiac-like cell [...] Read more.
Coxsackievirus B3 (CVB3) belongs to the enteroviruses, which are a well-known cause of acute and chronic myocarditis, primarily infecting cardiac myocytes. As primary human cardiomyocytes are difficult to obtain, viral myocarditis is quite frequently studied in vitro in different non-cardiac and cardiac-like cell lines. Recently, cardiomyocytes that have been differentiated from human-induced pluripotent stem cells have been described as a new model system to study CVB3 infection. Here, we compared iCell® Cardiomyocytes with other cell lines that are commonly used to study CVB3 infection regarding their susceptibility and patterns of infection and the mode of cell death. iCell® Cardiomyocytes, HeLa cells, HL-1 cells and H9c2 cells were infected with CVB3 (Nancy strain). The viral load, CVB3 RNA genome localization, VP1 expression (including the intracellular localization), cellular morphology and the expression of cell death markers were compared. The various cell lines clearly differed in their permissiveness to CVB3 infection, patterns of infection, viral load, and mode of cell death. When studying the mode of cell death of CVB3-infected iCell® Cardiomyocytes in more detail, especially regarding the necroptosis key players RIPK1 and RIPK3, we found that RIPK1 is cleaved during CVB3 infection. iCell® Cardiomyocytes represent well the natural host of CVB3 in the heart and are thus the most appropriate model system to study molecular mechanisms of CVB3-induced myocarditis in vitro. Doubts are raised about the suitability of commonly used cell lines such as HeLa cells, HL-1 cells and H9c2 cells to evaluate molecular pathways and processes occurring in vivo in enteroviral myocarditis. Full article
(This article belongs to the Special Issue Virus-Induced Myocarditis)
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15 pages, 3394 KiB  
Article
Exploration of Analgesia with Tramadol in the Coxsackievirus B3 Myocarditis Mouse Model
by Sandra Pinkert, Meike Kespohl, Nicolas Kelm, Ziya Kaya, Arnd Heuser, Karin Klingel and Antje Beling
Viruses 2021, 13(7), 1222; https://doi.org/10.3390/v13071222 - 24 Jun 2021
Cited by 2 | Viewed by 2687
Abstract
Infection of mice with Coxsackievirus B3 (CVB3) triggers inflammation of the heart and this mouse model is commonly used to investigate underlying mechanisms and therapeutic aspects for viral myocarditis. Virus-triggered cytotoxicity and the activity of infiltrating immune cells contribute to cardiac tissue injury. [...] Read more.
Infection of mice with Coxsackievirus B3 (CVB3) triggers inflammation of the heart and this mouse model is commonly used to investigate underlying mechanisms and therapeutic aspects for viral myocarditis. Virus-triggered cytotoxicity and the activity of infiltrating immune cells contribute to cardiac tissue injury. In addition to cardiac manifestation, CVB3 causes cell death and inflammation in the pancreas. The resulting pancreatitis represents a severe burden and under such experimental conditions, analgesics may be supportive to improve the animals’ well-being. Notably, several known mechanisms exist by which analgesics can interfere with the immune system and thereby compromise the feasibility of the model. We set up a study aiming to improve animal welfare while ensuring model integrity and investigated how tramadol, an opioid, affects virus-induced pathogenicity and immune response in the heart. Tramadol was administered seven days prior to a CVB3 infection in C57BL/6 mice and treatment was continued until the day of analysis. Tramadol had no effect on the virus titer or viral pathogenicity in the heart tissue and the inflammatory response, a hallmark of myocardial injury, was maintained. Our results show that tramadol exerts no disruptive effects on the CVB3 myocarditis mouse model and, therefore, the demonstrated protocol should be considered as a general analgesic strategy for CVB3 infection. Full article
(This article belongs to the Special Issue Virus-Induced Myocarditis)
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Review

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17 pages, 1949 KiB  
Review
Mitochondria Dysfunction at the Heart of Viral Myocarditis: Mechanistic Insights and Therapeutic Implications
by Yasir Mohamud, Boaz Li, Amirhossein Bahreyni and Honglin Luo
Viruses 2023, 15(2), 351; https://doi.org/10.3390/v15020351 - 26 Jan 2023
Cited by 14 | Viewed by 3358
Abstract
The myocardium/heart is the most mitochondria-rich tissue in the human body with mitochondria comprising approximately 30% of total cardiomyocyte volume. As the resident “powerhouse” of cells, mitochondria help to fuel the high energy demands of a continuously beating myocardium. It is no surprise [...] Read more.
The myocardium/heart is the most mitochondria-rich tissue in the human body with mitochondria comprising approximately 30% of total cardiomyocyte volume. As the resident “powerhouse” of cells, mitochondria help to fuel the high energy demands of a continuously beating myocardium. It is no surprise that mitochondrial dysfunction underscores the pathogenesis of many cardiovascular ailments, including those of viral origin such as virus-induced myocarditis. Enteroviruses have been especially linked to injuries of the myocardium and its sequelae dilated cardiomyopathy for which no effective therapies currently exist. Intriguingly, recent mechanistic insights have demonstrated viral infections to directly damage mitochondria, impair the mitochondrial quality control processes of the cell, such as disrupting mitochondrial antiviral innate immune signaling, and promoting mitochondrial-dependent pathological inflammation of the infected myocardium. In this review, we briefly highlight recent insights on the virus-mitochondria crosstalk and discuss the therapeutic implications of targeting mitochondria to preserve heart function and ultimately combat viral myocarditis. Full article
(This article belongs to the Special Issue Virus-Induced Myocarditis)
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33 pages, 4521 KiB  
Review
Toll-Like Receptors: Are They Taking a Toll on the Heart in Viral Myocarditis?
by Kasper Favere, Matthias Bosman, Karin Klingel, Stephane Heymans, Sophie Van Linthout, Peter L. Delputte, Johan De Sutter, Hein Heidbuchel and Pieter-Jan Guns
Viruses 2021, 13(6), 1003; https://doi.org/10.3390/v13061003 - 27 May 2021
Cited by 12 | Viewed by 4183
Abstract
Myocarditis is an inflammatory disease of the heart with viral infections being the most common aetiology. Its complex biology remains poorly understood and its clinical management is one of the most challenging in the field of cardiology. Toll-like receptors (TLRs), a family of [...] Read more.
Myocarditis is an inflammatory disease of the heart with viral infections being the most common aetiology. Its complex biology remains poorly understood and its clinical management is one of the most challenging in the field of cardiology. Toll-like receptors (TLRs), a family of evolutionarily conserved pattern recognition receptors, are increasingly known to be implicated in the pathophysiology of viral myocarditis. Their central role in innate and adaptive immune responses, and in the inflammatory reaction that ensues, indeed makes them prime candidates to profoundly affect every stage of the disease process. This review describes the pathogenesis and pathophysiology of viral myocarditis, and scrutinises the role of TLRs in every phase. We conclude with directions for future research in this field. Full article
(This article belongs to the Special Issue Virus-Induced Myocarditis)
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