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δ是一种亲肝性因子,其抗原/抗体系统(δ抗原/抗-δ)的表现度依赖于HBV。推定的整组基因是一种低分子量RNA,与HBV的DNA整组基因无分子关系。δ有高度致病性,是急、慢性肝病的病因。HBV和δ双重感染引起的肝炎较单由HBV引起的肝炎严重,致病力可能取决于HBV感染是否先于δ感染。为评价人类急性δ肝炎的临床严重度,本文作者检查了一组选自意大利、法国和英国的呈良性经过的乙型肝炎(BHB)和呈暴发性经过的乙型肝炎(FHB)患者δ感染的流行率。依据血清转氨酶水平超过正常10倍和HBsAg阳性而确诊的急性乙型肝炎患者643例,住院检测δ感染的血清学标志。肝炎为自限性,且无并发症,血清HBsAg于起病后1～2个月内阴转,定为BHB(532例);肝炎起病后4周内发生肝衰竭和昏迷,诊断
δ is a pro-hepatic factor whose expression of its antigen / antibody system (δ antigen / anti-δ) is dependent on HBV. The putative whole group of genes is a low-molecular weight RNA that has no molecular relationship to the entire set of HBV DNA. δ is highly pathogenic, is the cause of acute and chronic liver disease. Hepatitis B caused by HBV and δ double infection is more serious than hepatitis B caused by HBV alone. The pathogenicity may depend on whether HBV infection precedes δ infection. To assess the clinical severity of acute hepatitis in humans, the authors examined a panel of patients with benign infection of hepatitis B (BHB) and fulminant hepatitis B (FHB) patients from Italy, France and the United Kingdom The prevalence. 643 patients with acute hepatitis B diagnosed on the basis of a serum transaminase level 10 times higher than that of normal HBsAg positive patients were hospitalized for the serological detection of δ-infection. Hepatitis was self-limiting and had no complications. Serum HBsAg was negative for 1 to 2 months after onset and was defined as BHB (532 cases). Hepatic failure and coma occurred within 4 weeks after the onset of hepatitis