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提示HBeAg缺陷性乙型肝炎病毒(HBV)存在的最初证据是在抗-HBe阳性患者血清中出乎意料地检测到HBV DNA。这些患者可表现为严重的慢性肝炎,并对治疗呈特殊反应。其后发现了与HBeAg缺乏有关的基因变异,即由于单一碱基的突变(第1896位核苷酸上的鸟嘌呤为腺嘌呤所取代),结果产生了一个终止密码子(TAG),后者阻止了HBeAg的分泌。从意大利、希腊、日本、中国、印度尼西亚、肯尼亚、土耳其及保加利亚毫无关联的患者中分离出的HBV DNA,以强有力的证据支持一种特殊
The initial evidence suggesting the existence of HBeAg-deficient hepatitis B virus (HBV) was the unexpected detection of HBV DNA in sera of anti-HBe-positive patients. These patients can present with severe chronic hepatitis and respond specifically to treatment. Subsequent discovery of a genetic variant associated with HBeAg deficiency resulted in a stop codon (TAG) as a result of a single base mutation (guanine at the 1896th nucleotide was replaced by adenine), the latter Prevent HBeAg secretion. HBV DNA isolated from unrelated patients in Italy, Greece, Japan, China, Indonesia, Kenya, Turkey and Bulgaria strongly supports a special