探討細小病毒科病毒殼體蛋白獨立區域對H9c2心肌細胞的影響

人類微小病毒B19 (Human parvovirus B19, B19V) 和人類博卡病毒 (Human Bocavirus, HBoV) 屬於細小病毒科，殼體蛋白皆是由其VP1及VP2組成。在B19-VP1的N端比B19-VP2多了227個胺基酸序列;在HBoV-VP1比HBoV-VP2多了129個胺基酸序列，這區域都被稱為VP1-unique region (VP1u)，並具有sPLA2的活性。文獻指出，B19感染與許多心臟疾病有關，例如: 心肌炎，心肌病和心包炎。而B19V-VP1u已知是B19V感染人類的關鍵，並且其sPLA2活性與B19病毒感染所造成的疾病相關，例如:心肌炎。因此，本研究探討細小病毒科病毒殼體蛋白獨立區域對H9c2心肌細胞的影響。實驗結果發現B19V-VP1u會增進H9c2心肌細胞產生發炎反應並且和sPLA2活性有關。所以，B19V-VP1u的sPLA2活性可能是引起心肌炎的其中一種機制。

Human parvovirus B19 (B19V) and Human Bocavirus (HBoV) belong to Parvovirdae. Their capsids consist of two structural proteins, VP1 and VP2. In the end of the B19V-VP1 protein are identical except for 227 amino acids and at the end of the HBoV-VP1 protein are identical except for 129 amino acids, which are called VP1-unique region (VP1u), both of them contain sPLA2 enzyme activity. Previous studies show that B19V may trigger heart disease, such as myocarditis, cardiomyopathy, and pericarditis. Moreover, B19V-VP1u play an important role in B19V infection and its sPLA2 activity is related to the disease, such as myocarditis. Therefore, we intend to investigate the effects of the Parvovirdae capsid protein on H9c2 cardiomyocytes. Here, we report that inflammatory damage induced by B19V-VP1u with sPLA2 activity in cardiac H9c2 cells. Therefore, the sPLA2 activity of VP1u may involve the mechanisms of B19V-related myocarditis.