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      Roles of Host Immunity in Viral Myocarditis and Dilated Cardiomyopathy

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      Author(s): 1 , 2 , 3 ,
      Publication date (Electronic):
      Journal: Journal of Immunology Research
      Publisher: Hindawi

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          Abstract

          The pathogenesis of viral myocarditis includes both the direct damage mediated by viral infection and the indirect lesion resulted from host immune responses. Myocarditis can progress into dilated cardiomyopathy that is also associated with immunopathogenesis. T cell-mediated autoimmunity, antibody-mediated autoimmunity (autoantibodies), and innate immunity, working together, contribute to the development of myocarditis and dilated cardiomyopathy.

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          Myocarditis.

          Sandeep Sagar, Peter P Liu, Leslie Cooper (2012)
          Myocarditis is an underdiagnosed cause of acute heart failure, sudden death, and chronic dilated cardiomyopathy. In developed countries, viral infections commonly cause myocarditis; however, in the developing world, rheumatic carditis, Trypanosoma cruzi, and bacterial infections such as diphtheria still contribute to the global burden of the disease. The short-term prognosis of acute myocarditis is usually good, but varies widely by cause. Those patients who initially recover might develop recurrent dilated cardiomyopathy and heart failure, sometimes years later. Because myocarditis presents with non-specific symptoms including chest pain, dyspnoea, and palpitations, it often mimics more common disorders such as coronary artery disease. In some patients, cardiac MRI and endomyocardial biopsy can help identify myocarditis, predict risk of cardiovascular events, and guide treatment. Finding effective therapies has been challenging because the pathogenesis of chronic dilated cardiomyopathy after viral myocarditis is complex and determined by host and viral genetics as well as environmental factors. Findings from recent clinical trials suggest that some patients with chronic inflammatory cardiomyopathy have a progressive clinical course despite standard medical care and might improve with a short course of immunosuppression. Copyright © 2012 Elsevier Ltd. All rights reserved.
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            Molecular mimicry, bystander activation, or viral persistence: infections and autoimmune disease.

            Robert Fujinami, Matthias G von Herrath, Urs Christen … (2006)
            Virus infections and autoimmune disease have long been linked. These infections often precede the occurrence of inflammation in the target organ. Several mechanisms often used to explain the association of autoimmunity and virus infection are molecular mimicry, bystander activation (with or without epitope spreading), and viral persistence. These mechanisms have been used separately or in various combinations to account for the immunopathology observed at the site of infection and/or sites of autoimmune disease, such as the brain, heart, and pancreas. These mechanisms are discussed in the context of multiple sclerosis, myocarditis, and diabetes, three immune-medicated diseases often linked with virus infections.
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              The emerging role of Toll-like receptor 4 in myocardial inflammation

              Y. Yang, J Lv, S. T. Jiang … (2016)
              Toll-like receptors (TLRs) are a family of pattern recognition receptors involved in cardiovascular diseases. Notably, numerous studies have demonstrated that TLR4 activates the expression of several of pro-inflammatory cytokine genes that play pivotal roles in myocardial inflammation, particularly myocarditis, myocardial infarction, ischemia-reperfusion injury, and heart failure. In addition, TLR4 is an emerging target for anti-inflammatory therapies. Given the significance of TLR4, it would be useful to summarize the current literature on the molecular mechanisms and roles of TLR4 in myocardial inflammation. Thus, in this review, we first introduce the basic knowledge of the TLR4 gene and describe the activation and signaling pathways of TLR4 in myocardial inflammation. Moreover, we highlight the recent progress of research on the involvement of TLR4 in myocardial inflammation. The information reviewed here may be useful to further experimental research and to increase the potential of TLR4 as a therapeutic target.
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                Author and article information

                Contributors
                Zhaoying Fu:
                ORCID: http://orcid.org/0000-0003-3226-2104
                Journal
                Journal ID (nlm-ta): J Immunol Res
                Journal ID (iso-abbrev): J Immunol Res
                Journal ID (publisher-id): JIR
                Title: Journal of Immunology Research
                Publisher: Hindawi
                ISSN (Print): 2314-8861
                ISSN (Electronic): 2314-7156
                Publication date Collection: 2018
                Publication date (Electronic): 7 May 2018
                Volume: 2018
                Electronic Location Identifier: 5301548
                Affiliations
                1Affiliated Hospital, Yan'an University, Yan'an, Shaanxi Province 716000, China
                2College of Medicine, Yan'an University, Yan'an, Shaanxi Province 716000, China
                3Institute of Molecular Biology and Immunology, Yan'an University, Yan'an, Shaanxi Province 716000, China
                Author notes

                Academic Editor: Lucia Conti

                Author information
                http://orcid.org/0000-0003-3226-2104
                Article
                DOI: 10.1155/2018/5301548
                PMC ID: 5964556
                PubMed ID: 29854842
                SO-VID: 9afddad1-1d6f-4b16-8ee1-9f44cc4e150a
                Copyright © Copyright © 2018 Lifang Zhao and Zhaoying Fu.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 7 December 2017
                Date revision received : 9 April 2018
                Date accepted : 19 April 2018
                Funding
                Funded by: Research and Development Projects of Shaanxi Province
                Award ID: 2016SF-280
                Funded by: National Natural Science Foundation of China
                Categories
                Subject: Review Article

                Data availability:

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