Blum H E, Moradpour D, vøn Weizsäcker F, Wieland S, Peters T, Rasenack J W
Abteilung Innere Medizin II, Medizinische Universitätsklinik Freiburg.
Z Gastroenterol. 1997 May;35(5):347-55.
Hepatitis B virus (HBV) mutants have recently been identified in patients with acute or fulminant as well as chronic infections. Naturally occurring mutations have been identified in all viral genes and regulatory elements, most notably in the genes coding for the structural envelope and nucleocapsid proteins. Mutations in the gene coding for the hepatitis B surface antigen (HBsAg) may result in infection or viral persistence despite the presence of antibodies against HBsAg (anti-HBs) ("vaccine escape" or "immune escape"). Mutations in the gene encoding the pre-core/ core protein (pre-core stop codon mutant) result in a loss of hepatitis B e antigen (HBeAg) and seroconversion to antibodies to HBeAg (anti-HBe) with persistence of HBV replication (HBeAg minus mutant). Mutations in the core gene may lead among others to an "immune escape" due to a T cell receptor antagonism. Mutations in the gene coding for the polymerase/reverse transcriptase can be associated with viral persistence or resistance to nucleoside analogues. Thus, HBV mutations may affect the natural course of infection, viral clearance and response to antiviral therapy. Apart from the precore/core stop codon mutations, the exact contribution of specific mutations to diagnosis and therapy of HBV infection as well as patient management in clinical practice remain to be established.
最近在急性、暴发性及慢性乙肝病毒（HBV）感染患者中发现了HBV突变体。在所有病毒基因和调控元件中均发现了自然发生的突变，最显著的是在编码结构包膜蛋白和核衣壳蛋白的基因中。编码乙肝表面抗原（HBsAg）的基因发生突变，可能导致尽管存在抗HBsAg抗体（抗-HBs），仍发生感染或病毒持续存在（“疫苗逃逸”或“免疫逃逸”）。编码前核心/核心蛋白的基因发生突变（前核心终止密码子突变体），会导致乙肝e抗原（HBeAg）丧失，并血清转化为抗HBeAg抗体（抗-HBe），同时HBV复制持续存在（HBeAg阴性突变体）。核心基因发生突变可能会因T细胞受体拮抗作用等导致“免疫逃逸”。编码聚合酶/逆转录酶的基因发生突变可能与病毒持续存在或对核苷类似物耐药有关。因此，HBV突变可能会影响感染的自然病程、病毒清除以及对抗病毒治疗的反应。除前核心/核心终止密码子突变外，特定突变对HBV感染的诊断和治疗以及临床实践中患者管理的确切作用仍有待确定。
