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B형 간염바이러스 감염에서 불투명 유리상 간세포(Groundglass hepatocyte)의 원인으로서 pre-S1 변이종의 의의
조용균 ( Yong Kyun Cho ),김병익 ( Byung Ik Kim ),배지철 ( Ji Cheul Pae ),박승하 ( Seung Ha Park ),김상훈 ( Sang Hoon Kim ),박정호 ( Jung Ho Park ),김홍주 ( Hong Joo Kim ),박동일 ( Dong Il Park ),김향 ( Hyang Kim ),성인경 ( In Kyu 대한내과학회 2005 대한내과학회지 Vol.69 No.4
Background : Ground glass hepatocytes are unique histological feature of chronic hepatitis B viral infection. The pre-S1 region of large surface protein has been shown to regulate assembly, processing, and secretion of HBsAg. The purpose of this study was to elucidate that a mutant form of pre-S1 affects this normal secretory pathway and is responsible for ground glass hepatocyte. Methods : We examined HBV sequences spanning the pre-S region from a patients with HBeAg positive chronic HBV infection. HBV DNA was extracted from serum, cloned, and sequenced and determined the intrahepatic viral composition by extracting HBV DNA from paraffin embedded liver tissue. To analyze the viral population of single groundglass hepatocytes, we used the technique of laser capture microdissection to isolate individual hepatocytes from biopsy specimen. Groundglass hepatocytes that stained positively with anti-HBs and normal hepatocytes were harvested individually and their subjected HBV DNA sequences were analyzed. To define the responsible mutations for the HBsAg secretion, we introduced the mutant gene into molecular clone of wildtype (adwR9) and assayed their HBsAg amounts in the transfected cell supernatants by ELISA. Results : Of 12 clones in serum analyzed, 9 clones had identical wild type sequences in the N-terminal region of the pre-S1 protein which plays an important role in the secretion and retention of HBV envelope proteins. One of the wild type clones has deletion within pre-S2 region. 3 identical mutant clones were isolated. Mutant type clones were predominant groundglass hepatocytes. Conclusions : We speculate that a mutant form of the HBV pre-S1 protein may result in the formation of ground-glass hepatocytes. Expression of abnormal pre-S1 may lead to its retention and accumulation within hepatocytes.(Korean J Med 69:357-363, 2005)