Hepatitis B virus basal core promoter mutations show lower replication fitness associated with cccDNA acetylation status
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- 作者：Lemonica Koumbia ; lemonica.koumbi@gmail.com" class="auth_mail" title="E-mail the corresponding author ; Teresa Pollicinob ; tpollicino@unime.it" class="auth_mail" title="E-mail the corresponding author ; Giovanni Raimondoc ; giovanni.raimondo@unime.it" class="auth_mail" title="E-mail the corresponding author ; Dimitrios Stampoulisd ; d.stampoulis@ucl.ac.uk" class="auth_mail" title="E-mail the corresponding author ; Salim Khakooe ; S.I.Khakoo@soton.ac.uk" class="auth_mail" title="E-mail the corresponding author ; Peter Karayiannisf ; karayiannis.p@unic.ac.cy" class="auth_mail" title="E-mail the corresponding author
- 关键词：BCP ; basal core promoter ; CHB ; chronic HBV ; cccDNA ; covalently closed circular DNA ; DNMT ; DNA methyltransferases ; DS DNA ; double stranded DNA ; HATs ; histone acetyltransferases ; HDAC1 ; class 1 histone deacetylase ; OC DNA ; open circular DNA ; ORFs ; open reading frames ; pgRNA ; pre-genomic RNA ; SS DNA ; single stranded DNA ; TSA ; Trichostatin
- 刊名：Virus Research
- 出版年：2016
- 出版时间：15 July 2016
- 年：2016
- 卷：220
- 期：Complete
- 页码：150-160
- 全文大小：1765 K
文摘
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Basal core promote (BCP) mutations of hepatitis B virus show low replication fitness.
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The precore mutations have no significant effect on viral replication.
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Viral replication capacity of mutants parallels cccDNA acetylation status.
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cccDNA is a target for methylation and is accompanied by DNMT1 upregulation.
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HBV mutants modulate viral replication via cccDNA epigenetic control.