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HBeAg与HBcAg约有75%共同的氨基酸序列,但HBeAg和HBcAg的二级结构不同,各有特异的抗原决定簇。HBeAg的功能不是很清楚的,因为在病毒的装配、复制或者感染中并不需要HBeAg。HBeAg不仅能通过胎盘诱导胎儿的免疫耐受,导致出生后的慢性HBV感染;HBeAg存在且水平高时,患者对HBV的免疫应答反应低,对抗病毒治疗的疗效差[1]。现就近来关于HBeAg导致HBV感染免疫耐受研究情况尤其在分子水平上发挥免疫调节作一综述。
HBeAg and HBcAg about 75% common amino acid sequence, but the secondary structure of HBeAg and HBcAg different, each has a specific antigenic determinant. The function of HBeAg is not well understood because HBeAg is not required for virus assembly, replication or infection. HBeAg not only induces fetal immune tolerance through the placenta, resulting in postnatal chronic HBV infection. In the presence of high levels of HBeAg, patients have a low immune response to HBV and poor efficacy against antiviral therapy [1]. Now on the recent study of HBeAg-induced immune tolerance of HBV infection, especially on the molecular level to play an immunomodulatory review.