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Authors: Krömmelbein, Natascha
Wiebusch, Lüder
Schiedner, Gudrun
Büscher, Nicole
Sauer, Caroline
Florin, Luise
Sehn, Elisabeth
Wolfrum, Uwe
Plachter, Bodo
Title: Adenovirus E1A/E1B transformed amniotic fluid cells support human cytomegalovirus replication
Online publication date: 5-Oct-2022
Year of first publication: 2016
Language: english
Abstract: The human cytomegalovirus (HCMV) replicates to high titers in primary human fibroblast cell cultures. A variety of primary human cells and some tumor-derived cell lines do also support permissive HCMV replication, yet at low levels. Cell lines established by transfection of the transforming functions of adenoviruses have been notoriously resistant to HCMV replication and progeny production. Here, we provide first-time evidence that a permanent cell line immortalized by adenovirus type 5 E1A and E1B (CAP) is supporting the full HCMV replication cycle and is releasing infectious progeny. The CAP cell line had previously been established from amniotic fluid cells which were likely derived from membranes of the developing fetus. These cells can be grown under serum-free conditions. HCMV efficiently penetrated CAP cells, expressed its immediate-early proteins and dispersed restrictive PML-bodies. Viral DNA replication was initiated and viral progeny became detectable by electron microscopy in CAP cells. Furthermore, infectious virus was released from CAP cells, yet to lower levels compared to fibroblasts. Subviral dense bodies were also secreted from CAP cells. The results show that E1A/E1B expression in transformed cells is not generally repressive to HCMV replication and that CAP cells may be a good substrate for dense body based vaccine production.
DDC: 610 Medizin
610 Medical sciences
Institution: Johannes Gutenberg-Universität Mainz
Department: FB 04 Medizin
FB 10 Biologie
Place: Mainz
Version: Published version
Publication type: Zeitschriftenaufsatz
License: CC BY
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Journal: Viruses
Pages or article number: Art. 37
Publisher: MDPI
Publisher place: Basel
Issue date: 2016
ISSN: 1999-4915
Publisher URL:
Publisher DOI: 10.3390/v8020037
Appears in collections:DFG-OA-Publizieren (2012 - 2017)

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