Coxsackievirus B3 (CVB3) of the enteroviruses of the family Picornaviridae is associated with a variety of acute and chronic forms of diseases including meningoencephalitis, insulin-dependent type I diabetes (IDDM) (Curr Diab Rep. 2010;10(5):350-6) and, importantly myocarditis (Eur Heart J. 2013;34(33):2636-48). Although most enterovirus infections are subclinical, these viruses are capable of inducing severe acute myocarditis which may lead to life-threatening arrhythmias. With the introduction of the in situ hybridization technique and polymerase chain reaction CVB3 RNA was not only detected in endomyocardial biopsies of patients with acute and chronic myocarditis but also in those suffering from dilated cardiomyopathy (Proc Natl Acad Sci U S A. 1987;84(17):6272-6; New Engl J Med 2000; 343, 1388-1398).
The pathogenic concept of enteroviral infection in the human heart was confirmed in various mouse models of CVB3-induced myocarditis, demonstrating that after acute infection CVB3, typically a cytolytic virus, is capable of evading the immunological surveillance, thus inducing a persistent infection of the myocardium in susceptible animals (Proc Natl Acad Sci U S A. 1992;89(1):314-8) which may also be associated with arrhythmias (FASEB J. 2013; 27(10):4108-21). The course of myocarditis proved to be highly dependent on cellular factors (J Virol. 2014 Jul 1;88(13):7345-56) and an early effective immune response including Natural Killer cells (J Pathol. 2014 May 5. doi: 10.1002/path.4369. [Epub ahead of print]). The dysregulation of the cellular metabolism in chronic CVB3 myocarditis involves processes of hemoxygenase-1 mediated oxidative stress (Cell Physiol Biochem. 2014; 33(1):52-66) and the induction of inflammatory cytokines and proteins such as connective tissue growth factor, CTGF (J Mol Med (Berl). 2008; 86(1):49-60) und osteopontin (Circ Res. 2009 104(7):851-9), which are decisive in remodelling processes of the heart following inflammation.
For the detection of CVB3 in human und murine tissue and cells Mediagnost provides an antibody, capable to detect highly specific and sensitive the viral capsid protein VP1 which was already shown in the following publications:
Freiberg F, Sauter M, Pinkert S, Govindarajan T, Kaldrack J, Thakkar M, Fechner H, Klingel K, Gotthardt M. Interspecies Differences in Virus Uptake versus Cardiac Function of the Coxsackievirus and Adenovirus Receptor. J Virol. 2014 Jul 1;88(13):7345-56.
Klingel K, Fabritius C, Sauter M, Göldner K, Stauch D, Kandolf R, Ettischer N, Gahlen S, Schönberger T, Ebner S, Makrigiannis AP, Bélanger S, Diefenbach A, Polić B, Pratschke J, Kotsch K. The Activating Receptor NKG2D of Natural Killer Cells Promotes Resistance against Enterovirus-Mediated Inflammatory Cardiomyopathy. J Pathol. 2014 May 5. doi: 10.1002/path.4369. [Epub ahead of print]
Ursu ON, Sauter M, Ettischer N, Kandolf R, Klingel K. Heme oxygenase-1 mediates oxidative stress and apoptosis in coxsackievirus B3-induced myocarditis. Cell Physiol Biochem. 2014;33(1):52-66.
Ettischer-Schmid N, Normann A, Sauter M, Kraft L, Kalbacher H, Kandolf R, Flehmig B, Klingel K. A new monoclonal antibody (Cox mAB 31A2) detects VP1 protein of coxsackievirus B3 with high sensitivity and specificity. Virchows Arch