Levrero M, Balsano C, Avantaggiati M L, Natoli G, De Marzio E, Will H
I Clinica Medica e Fondazione Andrea Cesalpino, Policlinico Umberto I, Roma, Italy.
Ital J Gastroenterol. 1991 Dec;23(9):576-83.
Several epidemiological studies have demonstrated a link between chronic B virus infection and primary hepatocellular carcinoma (PHC). HBV DNA sequence integrations into the host cell genome have often been observed in hepatocarcinoma tissues. However, since only in a few cases of PHC the target of HBV-DNA insertion has been identified, alternative mechanisms for HBV-induced hepatocyte transformation have been investigated. Like many other DNA viruses, the hepatitis B virus bears a transactivational potential. Both full length and truncated versions of HBV X protein are able to influence the expression of cellular nuclear protooncogenes c-fos and c-myc. A second transcriptional activator is encoded by the PreS/S region of HBV, but its activity on viral and cellular genes become evident only after dislocations from its downstream sequences. Thus, HBV is able to influence infected cell growth and differentiation using both native proteins, newly generated truncated proteins and virus-cell fusion polypeptides.
多项流行病学研究表明，慢性B病毒感染与原发性肝细胞癌（PHC）之间存在关联。在肝癌组织中经常观察到HBV DNA序列整合到宿主细胞基因组中。然而，由于仅在少数PHC病例中确定了HBV-DNA插入的靶点，因此人们对HBV诱导肝细胞转化的替代机制进行了研究。与许多其他DNA病毒一样，乙型肝炎病毒具有反式激活潜能。HBV X蛋白的全长和截短版本都能够影响细胞核原癌基因c-fos和c-myc的表达。HBV的PreS/S区域编码第二种转录激活因子，但其对病毒和细胞基因的活性仅在与其下游序列错位后才变得明显。因此，HBV能够利用天然蛋白、新产生的截短蛋白和病毒-细胞融合多肽来影响受感染细胞的生长和分化。
