H Bx protein is essential to initiate and maintain virus replicat

StephenW

J Hepatol. 2011 Mar 1. [Epub ahead of print]
Hepatitis B Virus X protein is essential to initiate and maintain virus
replication after infection. Lucifora J, Arzberger S, Durantel D, Belloni L,
Strubin M, Levrero M, Zoulim F, Hantz O, Protzer U. Institute of Virology,
Technische Universität München / Helmholtz Zentrum München, Trogerstrasse,
30, 81675 Munich, Germany.

Abstract
BACKGROUND AND AIMS: Molecular biology of Hepatitis B Virus (HBV) has been
extensively studied but the exact role of the hepatitis B X protein (HBx) in the
context of natural HBV infections remains unknown. METHODS: Primary human
hepatocytes and differentiated HepaRG cells allowing conditional trans
complementation of HBx were infected with wild type (HBV(wt)) or HBx deficient
(HBV(x-)) HBV particles and establishment of HBV replication was followed.
RESULTS: We observed that cells inoculated with HBx-deficient HBV particles
(HBV(x-)) did not lead to productive HBV infection contrary to cells inoculated
with wild type HBV particles (HBV(wt)). Although equal amounts of nuclear
covalently closed circular HBV-DNA (cccDNA) demonstrated comparable uptake and
nuclear import, active transcription was only observed from HBV(wt) genomes.
Transcomplementation of HBx was able to rescue transcription from the HBV(x-)
genome and led to antigen and virion secretion even weeks after infection.
Constant expression of HBx was necessary to maintain HBV antigen expression and
replication. Finally, we demonstrated that HBx is not packaged into virions
during assembly but is expressed after infection within the new host cell to
allow epigenetic control of HBV transcription from cccDNA. CONCLUSIONS: Our
results demonstrate that HBx is required to initiate and maintain HBV
replication and highlight HBx as the key regulator during the natural infection
process.Copyright © 2011 European Association for the Study of the Liver.
Published by Elsevier B.V. All rights reserved. PMID: 21376091 [PubMed - as
supplied by publisher]                           



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StephenW

Ĵ肝脏病杂志。 2011年3月1日。 [EPUB的提前打印]
乙型肝炎病毒X蛋白是必不可少的启动和维持病毒
复制后的感染。 Lucifora J号，Arzberger秒，Durantel研发，贝罗尼L时，
Strubin男，Levrero男，Zoulim男，汉茨澳，Protzer美国病毒学研究所，
慕尼黑工业大学/亥姆霍兹慕尼黑，Trogerstrasse，
30，81675慕尼黑，德国。

摘要
背景与目的：乙型肝炎病毒分子生物学（HBV）的已
广泛的研究，但对肝炎Bx的蛋白（HBx蛋白）中的确切作用
乙肝病毒感染的自然情况依然不明。方法：原代人
肝细胞和分化细胞，允许有条件的跨HepaRG
HBx基因的互补与野生型感染（乙肝病毒（重））或HBx基因缺陷
（乙肝病毒（的X））乙肝病毒颗粒和乙肝病毒复制的建立是遵循。
结果：我们观察到细胞HBx的缺陷接种乙肝病毒颗粒
（乙肝病毒（的X））并没有导致生产性HBV感染的细胞接种相反
与野生型HBV颗粒（乙肝病毒（重量））。虽然核等量
共价闭合环状的HBV - DNA（cccDNA的）表现出相当的吸收和
核进口，积极转录只观察到乙肝病毒（重量）的基因组。
HBx基因的Transcomplementation能够拯救乙肝病毒转录（的X）
基因组，并导致抗原和病毒感染后分泌甚至数周。
HBx基因的表达，常需要维持和HBV抗原的表达
复制。最后，我们证明HBx蛋白不进病毒颗粒包装
在装配过程中，但感染后表示，在新的宿主细胞
允许从乙肝病毒cccDNA的转录后生控制。结论：我们的
结果表明，HBx的是启动和维持所需的乙肝病毒
复制并突出HBx的监管为重点，在自然感染
process.Copyright ©用于2011年欧洲肝脏研究协会。
B.诉由Elsevier出版的所有权利保留。结论：21376091 [PubMed的 - 作为
出版商提供的]

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