Myocarditis is defined as an inflammation of myocardium where the infiltrating leukocytes are intimately associated with cardiomyocyte necrosis or drop-out (Liu, 2005; Woodruff, 1980). Cardiac damage may be minimal and self-limiting or may result in chronic fibrosis and cardiac dysfunction leading to death in children and young adults (Eckart et al., 2004; Fabre, 2006; Solberg et al., 2010). As discussed in other chapters of this book, infections with a highly diverse group of viruses, bacteria, fungi, and worms have been implicated in infectious myocarditis (Friman et al., 1995). Enteroviruses and adenoviruses are usually considered as the predominant viral etiological agents, and are associated with approximately 80% of clinical myocarditis where a viral infection is documented. However, virtually any virus infection may initiate myocarditis (Bowles et al., 2003; Woodruff, 1980). While seasonal influenza virus is only a minor etiological agent in myocarditis, evidence from the most recent influenza H1N1 pandemic (Vila de Muga et al., 2010; Wiegand et al., 2010; Zheng et al., 2010) suggests a higher incidence of both mortality and morbidity, and accounts for 5% of complications in infected children (Zheng et al., 2010). Myocardial injury results either directly from replication and induction of death or dysfunction in infected cardiocytes, or from host responses to infection (Huber, 2010). Although anti-viral host responses (innate or adaptive) are intended to control and eliminate the infection, cytokines and by-products such as nitric oxide or oxygen free radicals may also damage adjacent uninfected cells (Szalay et al., 2006). Innate immunity is the initial host response to infection and usually occurs within hours or days of virus introduction. The major characteristic of the innate response, besides its rapidity, is that it is broadly reactive to multiple infectious agents. While it is highly unlikely that innate immunity can completely eliminate the infection, it can suppress microbial replication until the far more potent and highly specific adaptive immune response kicks in. The reason for this is quite simple, viruses replicate rapidly with, for example, one picornavirus infected cell in tissue culture producing up to a million progeny virions within 18-24 hrs. In vivo, such rapid and uncontrolled growth could result in extensive tissue injury or death of the organism prior to a useful adaptive immune response being established since during a primary immune response, production of meaningful numbers of virus-specific T cells could www.intechopen.com Myocarditis 218 take 7-10 days after virus inoculation. The best known innate immunity results from microbial products binding to and activating Toll-Like Receptors (TLR) or RNA helicases (RIG-I and MDA-5) which activate transcription factors (NFkB) leading to expression of cytokines (TNF , IL-1 and IL-6) and nitric oxide (Hosoi et al., 2004; Michelsen et al., 2004); or interferon response factors (IRF3/7) leading to expression of type 1 interferons (IFN /) ...
