| Summary: | 碩士 === 中山醫學大學 === 免疫學研究所 === 98 === Human parvovirus B19 is one of the Parvoviridae family and known to be pathologic in humans. The capsid of parvovirus B19 consists of two structural proteins, VP1 and VP2, which are identical except for 227 amino acids at the amino-terminal end of the VP1 protein. So the additional 227 amino acids at VP1 amino-terminus were called VP1-unique region (VP1u). Recently, more and more literatures assumed that there is a link between B19 infection and myocarditis, but the detailed mechanisms are still unknown. In addition, parvovirus B19 infection has been associated with autoimmune diseases including SLE. Some studies have supposed that B19 may exacerbate or even induce SLE. In recent research, B19 VP1u was discovered that the region played an important role in successful infection and inflammation response. However, fewer literatures discussed whether B19 VP1u could cause myocarditis. In this study, we used NZB/W F1 mice as a lupus-prone model and inoculated these mice with (1) PBS, (2) Rabbit IgG and (3) Rabbit anit-B19 VP1u IgG respectively. We found that NZB/W F1 mice inoculated with B19-VP1u IgG had higher Aspartate Aminotransferase level in sera. Besides, we found that B19-VP1u IgG promoted protein expression and activity of matrix metalloproteinase 9 in heart via NFκB pathway. Moreover, B19 VP1u IgG didn’t cause myocardial infarction or hypertrophy. All together, we supposed that B19-VP1u IgG inoculation might directly or indirectly cause mice myocardial damage. In conclusion, anti-B19 VP1u IgG inoculation not only aggravates disease activity of SLE, but also causes cardiac damage and inflammation.
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