Uchida T, Shimojima M, Gotoh K, Shikata T, Tanaka E, Kiyosawa K
Department of Pathology, Nihon University School of Medicine, Tokyo, Japan.
Microbiol Immunol. 1994;38(4):281-5. doi: 10.1111/j.1348-0421.1994.tb01777.x.
Since the recent introduction of diagnostic kits for hepatitis C and E, some cases of non-A, non-B, non-C, non-D, non-E hepatitis (so-called hepatitis F) have been revealed. We attempted to demonstrate that so-called hepatitis F is caused by hepatitis B virus (HBV) variants. Polymerase chain reaction (PCR) was used to amplify serum HBV DNAs from 20 patients with acute hepatitis and 20 patients with chronic hepatitis who had been diagnosed as having so-called hepatitis F on the basis of conventional serological markers. The PCR technique successfully amplified HBV DNAs in 18 (90%) cases of acute hepatitis and 17 (85%) cases of chronic hepatitis. Sequencing of HBV DNAs of six patients (acute 3, chronic 3) revealed equally a T-to-C mutation of DR2 and an 8-nucleotide deletion of the 3'-terminus of the X gene coding region, giving rise to the generation of a C-terminally truncated X protein and probable damage to the enhancer II/core promoter elements. These mutations of the X gene coding region may lead to suppression of replication and expression of HBV DNAs. Thus virtually all cases of so-called hepatitis F appear to be caused by "silent" HBV mutants, at least in Japan.
自从最近引入丙型和戊型肝炎诊断试剂盒以来，一些非甲、非乙、非丙、非丁、非戊型肝炎病例（即所谓的庚型肝炎）被发现。我们试图证明所谓的庚型肝炎是由乙型肝炎病毒（HBV）变异体引起的。采用聚合酶链反应（PCR）从20例急性肝炎患者和20例慢性肝炎患者的血清中扩增HBV DNA，这些患者根据传统血清学标志物被诊断为患有所谓的庚型肝炎。PCR技术成功扩增了18例（90%）急性肝炎患者和17例（85%）慢性肝炎患者的HBV DNA。对6例患者（急性3例，慢性3例）的HBV DNA进行测序，同样发现DR2区域存在T到C的突变以及X基因编码区3'末端有8个核苷酸的缺失，导致产生C末端截短的X蛋白，并可能损害增强子II/核心启动子元件。X基因编码区的这些突变可能导致HBV DNA复制和表达受到抑制。因此，至少在日本，几乎所有所谓的庚型肝炎病例似乎都是由“沉默”的HBV突变体引起的。
