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发表于 2014-9-2 20:36 |只看该作者 |倒序浏览 |打印
Occult hepatitis B infection
Teresa Pollicino email
,
Giovanni Raimondo email
Received: January 12, 2014; Received in revised form: April 21, 2014; Accepted: April 24, 2014; Published Online: June 26, 2014
DOI: http://dx.doi.org/10.1016/j.jhep.2014.04.036

   
Keywords:
Occult HBV infection, Immunological control of HBV, Epigenetic control of HBV, Clinical implication of occult HBV infection

Occult hepatitis B virus (HBV) infection (OBI) is recognized as one of the possible phases in the natural history of chronic HBV infection [1]. OBI defines the persistence of HBV genomes in the hepatocytes of individuals testing negative for HBV surface antigen (HBsAg) and, usually, also for serum HBV DNA [2]. Apart from some cases in which the lack of HBsAg detection is attributable to the HBV genetic heterogeneity (i.e., infection with replication-defective variants or with S-escape mutants producing a modified HBsAg undetectable by diagnostic kits), in most cases OBI is related to replication-competent viruses that are strongly suppressed in their activities (replicative and transcriptional) by the host’s defense mechanisms. Very importantly, this suppression (a) does not have an absolute effect and residual, low-levels of replication and transcription may persist over time, and (b) may be reversible in particular circumstances leading to viral reactivation and development of a typical HBsAg-positive (namely, “overt”) infection [[3], [4], [5], [6], [7], [8], [9], [10], [11], [12], [13], [14]].

隐匿性乙肝病毒感染
邓丽君Pollicino电子邮件

乔瓦尼·雷蒙电子邮件
收稿日期:2014年1月12日;收到修改稿:2014年4月21日;接受日期:2014年4月24日;发表时间:2014年6月26日
DOI:http://dx.doi.org/10.1016/j.jhep.2014.04.036

   
关键词:
隐匿性HBV感染,免疫控制乙肝病毒,乙肝病毒的表观遗传调控,隐匿性HBV感染的临床意义

隐匿性乙型肝炎病毒(HBV)感染(OBI)被公认为是可能的相位中的一个在慢性HBV感染[1]的自然历史。 OBI定义的HBV基因组的持久性在个体试验阴性的HBV表面抗原(HBsAg)和通常的肝细胞,也为血清HBV DNA[2]。除了某些情况下,其中缺乏的HBsAg检测是归属于HBV的遗传异质性(即感染与复制缺陷型变异体或具有生产改性的HBsAg检不出的诊断试剂盒的S-逃避突变型),在大多数情况下,OBI涉及被强烈抑制其活动(复制和转录)主机的防御机制复制能力的病毒。非常重要的是,这种抑制(a)不具有绝对影响和残余的低级别的复制和转录的可能持续时间的推移,及(b)可以是可逆的,导致病毒的再活化的典型HBsAg-的和发展的特殊情况正面(即,“公开”)的感染[[3],[4],[5],[6],[7],[8],[9],[10],[11],[12], [13],[14]。

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发表于 2014-9-2 20:42 |只看该作者


Fig. 1

Schematic comparison of overt and occult HBV infection. Mechanisms potentially involved in HBV inhibition and OBI induction are summarized. In particular, immunological (presence of functionally efficient central/effector memory T cells), genetic (HBV genomic variability, APOBEC hyperediting), epigenetic (methylation of CpG-rich regions within the HBV genome as well as acetylation/methylation of cccDNA-bound histones and recruitment of chromatin modifying enzymes onto the viral minichromosome) and co-/posttranscriptional (HBV RNA splicing, HBV replication inhibition by cellular miRNAs and by editing-independent functions of the cellular APOBEC3 proteins) mechanisms are represented. Differences in nucleosomal packaging and transcriptional activity of HBV minichromosomes as well as in amounts of total viral DNA, transcripts, proteins and virion formation and secretion are also displayed. DC, Dendritic Cell; CD4, CD4+ T cell; CD8, CD8+ T cell; RC DNA, Relaxed Circular DNA; cccDNA, covalently closed circular DNA; pgRNA, pregenomic RNA; HBs, envelope proteins; SVPs, subviral particles; TF, cellular transcription factors; HATs, histone acetyl transferases; HMT, histone methyltransferases; APOBEC3, apo B mRNA editing enzyme catalytic polypeptide; hnRNP K, heterogeneous nuclear ribonucleoprotein K; miRNAs, microRNAs; CpG meth, methylated CpG islands.

Fig。1

显性和隐匿性HBV感染的比较示意图。机制可能参与乙肝病毒的抑制和诱导欧倍德进行了总结。特别是,免疫(存在功能上有效的中央/效应记忆T细胞),基因(HBV基因组的变异性,APOBEC hyperediting),表观遗传(HBV基因组中的甲基化CpG富集区域以及乙酰化/ cccDNA的结合组蛋白的甲基化和招募染色质修饰酶到病毒微染色体)和助/转录后(HBV RNA剪接,乙型肝炎病毒复制的抑制通过细胞的miRNA以及由蜂窝APOBEC3蛋白质编辑无关的功能)机制来表示。在核小体的包装和在总病毒DNA,转录物,蛋白和病毒粒子的形成和分泌的量的HBV微染色体以及转录活性的差异也被显示。 DC,树突细胞; CD4 +,CD4 + T细胞; CD8,CD8 + T细胞;钢筋混凝土的DNA,轻松环状DNA; cccDNA的,共价闭合环状DNA; pgRNA,前基因组RNA; HBs抗体,包膜蛋白;的SVP,亚病毒颗粒; TF,细胞转录因子;帽子,组蛋白乙酰转移酶; HMT,组蛋白甲基转移; APOBEC3,载脂蛋白B的mRNA编辑酶催化多肽;核蛋白K,异质核核糖核蛋白k;微RNA,微RNA;甲基化CpG甲基化CpG岛。

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发表于 2014-9-2 20:46 |只看该作者

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发表于 2014-9-3 08:22 |只看该作者
万变不离其宗,我认为,能被称为乙肝病毒,他再怎么变异,都有其不变的特性,否则变异后,就应该是检测不到乙肝病毒了。而是另一种病毒

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发表于 2014-9-3 12:12 |只看该作者
回复 kite2002005 的帖子

同意你的观点,悟空纵有千变万化,也难隐藏他那根猴尾!
我的干扰治疗记录   予人玫瑰,手有余香
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