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柯萨奇B组病毒是引起病毒性心肌炎的主要病原之一,有25％VMC患者的确切病因是由CVB感染所致。根据其对新生乳鼠的致病特点,CVB可分为六个血清型,其中CVB3有很强的噬心肌性,在病变心肌组织中发现的CVB3病毒RNA序列已经证实这一点。通过研究CVB3病毒结构蛋白与疾病发病机理之间的关系,以及重组CVB3嵌合病毒与心血管疾病的相关位点,证实CVB3的5’端非编码区对病毒毒力的重要作用;同时证实除诱导心肌炎的病毒可以直接破坏感染细胞外,宿主的自发性免疫反应则使心肌组织进一步损伤,由于心肌纤维化、心肌细胞肥大以及心肌结构重塑,最终导致约15％的VMC患者可逐渐发展成为扩张型心肌病。
Coxsackie B virus is one of the major pathogens causing viral myocarditis. The exact cause of 25% of VMCs is due to CVB infection. According to its virulence characteristics of neonatal rats, CVB can be divided into six serotypes, including CVB3 has a strong cardiac muscle, found in diseased myocardium CVB3 virus RNA sequence has confirmed this point. By studying the relationship between structural proteins of CVB3 virus and the pathogenesis of CVB3 and the related sites of recombinant CVB3 chimeric virus and cardiovascular diseases, it was confirmed that the 5 ’non-coding region of CVB3 plays an important role in virus virulence. At the same time, The virus that induces myocarditis can destroy the infected cells directly, and the host’s spontaneous immune response causes further damage to the myocardium. Eventually, about 15% of VMC patients develop gradually due to myocardial fibrosis, cardiomyocyte hypertrophy and myocardial remodeling Dilated cardiomyopathy.