Gutenberg Open Science: Involvement of ESCRT-II in hepatitis B virus morphogenesis

Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-7575

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DC Field	Value	Language
dc.contributor.author	Stieler, Jens	-
dc.contributor.author	Prange, Reinhild	-
dc.date.accessioned	2022-08-19T08:33:50Z	-
dc.date.available	2022-08-19T08:33:50Z	-
dc.date.issued	2014
dc.identifier.uri	https://openscience.ub.uni-mainz.de/handle/20.500.12030/7589	-
dc.description.abstract	The hepatitis B virus (HBV) is an enveloped DNA virus that replicates via reverse transcription of its pregenomic RNA (pgRNA). Budding of HBV is supposed to occur at intracellular membranes and requires scission functions of the endosomal sorting complex required for transport (ESCRT) provided by ESCRT-III and VPS4. Here, we have investigated the impact of the upstream-acting ESCRT-I and ESCRT-II complexes in HBV morphogenesis. RNA interference knockdown of the ESCRT-I subunits TSG101 and VPS28 did not block, but rather stimulate virus release. In contrast, RNAi-mediated depletion of the ESCRT-II components EAP20, EAP30 and EAP45 greatly reduced virus egress. By analyzing different steps of the HBV maturation pathway, we find that the knockdown of ESCRT-II not only inhibited the production and/or release of enveloped virions, but also impaired intracellular nucleocapsid formation. Transcription/translation studies revealed that the depletion of ESCRT-II neither affected the synthesis and nuclear export of HBV-specific RNAs nor the expression of the viral core and envelope proteins. Moreover, the absence of ESCRT-II had no effects on the assembly capability and integrity of HBV core/capsids. However, the level of encapsidated pgRNA was significantly reduced in ESCRT-II-depleted cells, implicating that ESCRT-II directs steps accompanying the formation of replication-competent nucleocapsids, like e.g. assisting in RNA trafficking and encapsidation. In support of this, the capsid protein was found to interact and colocalize with ESCRT-II subunits in virus-producing cells. Together, these results indicate an essential role for ESCRT-II in the HBV life cycle and suggest that ESCRT-II functions prior to the final HBV budding reaction.	en_GB
dc.description.sponsorship	DFG, Open Access-Publizieren Universität Mainz / Universitätsmedizin	de
dc.language.iso	eng	de
dc.rights	CC BY	*
dc.rights.uri	https://creativecommons.org/licenses/by/4.0/	*
dc.subject.ddc	610 Medizin	de_DE
dc.subject.ddc	610 Medical sciences	en_GB
dc.title	Involvement of ESCRT-II in hepatitis B virus morphogenesis	en_GB
dc.type	Zeitschriftenaufsatz	de
dc.identifier.doi	http://doi.org/10.25358/openscience-7575	-
jgu.type.dinitype	article	en_GB
jgu.type.version	Published version	de
jgu.type.resource	Text	de
jgu.organisation.department	FB 04 Medizin	de
jgu.organisation.number	2700	-
jgu.organisation.name	Johannes Gutenberg-Universität Mainz	-
jgu.rights.accessrights	openAccess	-
jgu.journal.title	PLoS one	de
jgu.journal.volume	9	de
jgu.journal.issue	3	de
jgu.pages.alternative	e91279	de
jgu.publisher.year	2014	-
jgu.publisher.name	PLoS	de
jgu.publisher.place	Lawrence, Kan.	de
jgu.publisher.uri	http://dx.doi.org/10.1371/journal.pone.0091279	de
jgu.publisher.issn	1932-6203	de
jgu.organisation.place	Mainz	-
jgu.identifier.pmid	24614091
jgu.subject.ddccode	610	de
opus.date.modified	2018-08-08T08:47:54Z
opus.subject.dfgcode	00-000
opus.organisation.string	FB 04: Medizin: Institut für Medizinische Mikrobiologie und Hygiene	de_DE
opus.identifier.opusid	27340
opus.importsource	pubmed
opus.institute.number	0408
opus.metadataonly	false
opus.type.contenttype	Keine	de_DE
opus.type.contenttype	None	en_EN
opus.affiliated	Stieler, Jens
opus.affiliated	Prange, Reinhild
jgu.publisher.doi	10.1371/journal.pone.0091279	de
jgu.organisation.ror	https://ror.org/023b0x485	-
Appears in collections:	DFG-OA-Publizieren (2012 - 2017)

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