Chronic leukocytoclastic vasculitis complicating HBV infection. Possible role of mutant forms of HBV in pathogenesis and persistence of disease.
Chronic leukocytoclastic vasculitis complicating HBV infection. Possible role of mutant forms of HBV in pathogenesis and persistence of disease.
复制标题
乙型肝炎病毒感染并发慢性白细胞破碎性血管炎。
DOI：
10.1097/00004836-199507000-00011
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发表时间：
1995
影响因子：
2.9
通讯作者：
Banner,B
中科院分区：
文献类型：
--
作者：
Bonkovsky,HL;Liang,TJ;Hasegawa,K;Banner,B
一名年轻女子发展关节炎和白细胞破碎性血管炎，其次是肝炎由于前核心突变株的B型肝炎病毒（HBV）不能合成HBe抗原。丙型肝炎病毒抗体检测持续阴性。用α干扰素治疗患者最初导致肝炎严重恶化。后来，更高剂量的干扰素被耐受，并与HBV复制减少和肝组织病理学和血清转氨酶的改善相关。干扰素治疗后，重复肝活检的HBV DNA测序显示一组新的突变，这可能导致病毒蛋白免疫显性表位的改变。研究结果表明，HBV的“自然发生”突变形式与患者的慢性肝炎和血管炎有关，并且干扰素治疗对HBV产生的免疫压力可能导致病毒基因组中的其他突变，并持续存在低水平HBV感染。
A young woman developed arthritis and leukocytoclastic vasculitis, followed by hepatitis due to a precore mutant strain of hepatitis B virus (HBV) incapable of synthesizing HBe antigen. Tests for antibodies to HCV were persistently negative. Treatment of the patient with alpha interferon initially led to a severe exacerbation of hepatitis. Later, higher doses of interferon were tolerated and were associated with reduction of HBV replication and improvement in liver histopathology and serum aminotransferases. After interferon therapy, sequencing of HBV DNA from a repeat liver biopsy showed a cluster of new mutations, which may have led to alterations in immunodominant epitopes of viral proteins. The findings suggest that a" naturally occurring" mutant form of HBV was associated with chronic hepatitis and vasculitis in the patient, and that the immunological pressure on HBV produced by therapy with interferon may have led to other mutations in the viral genome with persistence of low-level HBV infection.