What we learned from pandemic H1N1 influenza A

Abstract

This editorial refers to ‘Up-regulation of ectopic trypsins in the myocardium by influenza A virus infection triggers acute myocarditis’ by H.-Y. Pan et al ., pp. 595–603, this issue. Myocarditis is defined as inflammation of the heart muscle, and it frequently associates with impaired cardiac function. Although many kinds of viruses have been implicated as causes of myocarditis, these most commonly include enteroviruses, such as coxsackieviruses. Beside enteroviruses, adenovirus, hepatitis virus, parvovirus, and influenza virus have been reported to cause myocarditis.1 Of the viruses that cause myocarditis, the cellular and molecular mechanisms of myocarditis induced by coxsackievirus infection have been most thoroughly investigated with murine models.2 In 1999, the importance of enteroviral protease 2A was reported as a cause of acquired cardiomyopathy associated with coxsackievirus B3 (CVB3) myocarditis.3 However, the molecular mechanisms of myocarditis induced by influenza virus have not been fully clarified. The study reported by Pan et al. 4 is a continuation of their previous study demonstrating that influenza A virus (IAV) infection increased the ectopic trypsin expression in the brain. They further examined the molecular mechanism …