HBV感染中抗-(抗-HBs)独特型抗体的研究

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1.75%聚乙二醇(MW6000)沉淀血清免疫复合物后,采用ELISA法检测上清中抗独特型抗体〔抗-(抗-HBs)〕。56例急性HBV感染患者血清IgM抗-(抗-HBs),第一周检出率最高(60.00%),1个月后大部分阴性,IgG抗-(抗-HBs)维持时间略长。IgM抗-(抗-HBs)较HBsAg/IgM和IgM抗-HBc消失早,将有利于急性HBV感染的诊断。27例CAH和29例CPH,IgM和IgG抗-(抗-HBs)阳性率约为38~52%,两型间无显著差异(p>0.5)。3例无症状HBsAg携带者和12例HBsAg血清疫苗接受者血清,抗-(抗-HBs)阴性。115例HBV感染者中,IgM抗-(抗-HBs)阳性者HBsAg阳性率(93.62)显著高于IgM抗-(抗-HBs)阴性者(52.31%),p<0.005;反之,HBsAg阳性血清IgM抗-(抗-HBs)阳性率(55.5S%)显著高于HBsAg阴性血清(9.68%),p<0.005;IgM抗-(抗-HBs)阳性和阴性血清的HBVDNA阳性率有显著差异(p<0.025),IgG反应到类似的结果。以上资料表明,抗-(抗-HBs)提示了一些HBV感染患者体内可能存在一种缺陷的反馈机制,导致抗-HBs产生不足而容许更活跃的HBV复制。本文证明了HBV感染患者血清中存在的抗-(抗-HBs)可能是共同决定簇“a”特异性的,还表明抗-HBs人抗-Id反应可能被纯化人血清HBsAg抑制,提示人抗-(抗-HBs)与抗-HBs结合的位点可能在HBsAg与抗-HBs结合位点内或在其附近,这和一些动物抗-(抗-HBs)的研究结果是一致的。 After anti-idiotypic antibody (anti-HBs) was detected in the supernatant by 1.75% polyethylene glycol (MW 6000) precipitation of serum immune complexes. The serum IgM anti - (anti - HBs) in 56 patients with acute HBV infection had the highest detection rate in the first week (60.00%), mostly negative after one month and the IgG anti - (HBs) maintenance time slightly longer. IgM anti - (anti-HBs) than HBsAg / IgM and IgM anti-HBc disappear early, will be conducive to the diagnosis of acute HBV infection. The positive rate of anti-HBs in 27 cases of CAH and 29 cases of CPH was about 38-52%. There was no significant difference between the two types (p> 0.5). Serum samples from 3 asymptomatic HBsAg carriers and 12 HBsAg vaccine recipients were negative for anti-(anti-HBs). The positive rate of HBsAg (93.62) was higher in IgM anti-HBs positive than that in IgM anti-HBs (52.31%), p <0.005. In contrast, HBsAg positive serum The positive rate of IgM anti-HBs (55.5S%) was significantly higher than that of HBsAg negative serum (9.68%), p <0.005. The positive rates of HBVDNA in IgM anti-HBs positive and negative sera were significantly different p <0.025), IgG reacted to similar results. The above data suggest that anti-(anti-HBs) suggests that there may be a defect feedback mechanism in some HBV-infected patients that leads to insufficient production of anti-HBs to allow for more active HBV replication. This paper demonstrates that the anti-HBs present in the sera of patients with HBV infection may be specific for the “a” determinant of co-determinants, and that human anti-Id responses to anti-HBs may be inhibited by purified human serum HBsAg, suggesting that human anti- - (anti-HBs) may bind to anti-HBs at or near the binding sites of HBsAg and anti-HBs, consistent with the findings of some animal anti-(anti-HBs) studies.
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