Division of Cardiology, Department of Medicine, University of California, San Diego, La Jolla, 92093-0613K, USA.
Future Microbiol. 2011 May;6(5):551-66. doi: 10.2217/fmb.11.40.
Virus infection can inflict significant damage on cardiomyocytes through direct injury and secondary immune reactions, leading to myocarditis and dilated cardiomyopathy. While viral myocarditis or cardiomyopathy is a complication of systemic infection of cardiotropic viruses, most individuals infected with the viruses do not develop significant cardiac disease. However, some individuals proceed to develop severe virus-mediated heart disease. Recent studies have shown that viral infection of cardiomyocytes is required for the development of myocarditis and subsequent cardiomyopathy. This suggests that viral infection of cardiomyocytes can be an important step that determines the pathogenesis of viral myocarditis during systemic infection. Accordingly, this article focuses on potential defense mechanisms within the cardiomyocyte against virus infection. Understanding of the cardiomyocyte defense against invading viruses may give us novel insights into the pathophysiology of viral myocarditis, and enable us to develop innovative strategies of diagnosis and treatment for this challenging clinical entity.
病毒感染可通过直接损伤和继发免疫反应对心肌细胞造成严重损害，导致心肌炎和扩张型心肌病。病毒性心肌炎或心肌病是心肌亲病毒全身感染的并发症，但大多数感染病毒的个体并不发生明显的心脏疾病。然而，一些个体进展为严重的病毒介导的心脏病。最近的研究表明，心肌细胞的病毒感染是心肌炎和随后的心肌病发展所必需的。这表明，心肌细胞的病毒感染可能是决定全身感染期间病毒性心肌炎发病机制的重要步骤。因此，本文重点介绍心肌细胞针对病毒感染的潜在防御机制。了解心肌细胞对入侵病毒的防御机制，可能使我们对病毒性心肌炎的病理生理学有新的认识，并使我们能够为这一具有挑战性的临床实体制定创新的诊断和治疗策略。
