LIVIVO - Search results -

Search results

Result 1 - 10 of total 148

Article: In vitro

Guo, Hongbo / Urban, Stephan / Wang, Wenshi

2023 Volume 14, Page(s) 1169770

Abstract: Chronic infection with the hepatitis B virus (HBV) and hepatitis D virus (HDV) can cause a major global health burden. Current medication regimens can repress viral replication and help to control disease progression, but a complete cure is hardly ... ...

Abstract	Chronic infection with the hepatitis B virus (HBV) and hepatitis D virus (HDV) can cause a major global health burden. Current medication regimens can repress viral replication and help to control disease progression, but a complete cure is hardly achieved due to the difficulties to eradicate viral templates (cccDNA and integrates). To develop novel curative antiviral therapies for HBV/HDV infection, it is vital to precisely understand the details of the molecular biology of both viruses and the virus-host interactions. One important prerequisite for gaining this aim is the availability of suitable
Language	English
Publishing date	2023-04-05
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2587354-4
ISSN	1664-302X
ISSN	1664-302X
DOI	10.3389/fmicb.2023.1169770
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Article ; Online: Liver capsule: Entry and entry inhibition of hepatitis B virus and hepatitis delta virus into hepatocytes.

Urban, Stephan

Hepatology (Baltimore, Md.)

2016 Volume 63, Issue 2, Page(s) 633

MeSH term(s)	Hepatitis B virus/physiology ; Hepatitis Delta Virus/physiology ; Hepatocytes/virology ; Humans ; Virus Internalization
Language	English
Publishing date	2016-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1002/hep.28308
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 1660: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Medical Advances in Hepatitis D Therapy: Molecular Targets.

Vogt, Amelie / Wohlfart, Sabrina / Urban, Stephan / Mier, Walter

International journal of molecular sciences

2022 Volume 23, Issue 18

Abstract: An approximate number of 250 million people worldwide are chronically infected with hepatitis B virus, making them susceptible to a coinfection with hepatitis D virus. The superinfection causes the most severe form of a viral hepatitis and thus ... ...

Abstract	An approximate number of 250 million people worldwide are chronically infected with hepatitis B virus, making them susceptible to a coinfection with hepatitis D virus. The superinfection causes the most severe form of a viral hepatitis and thus drastically worsens the course of the disease. Until recently, the only available therapy consisted of interferon-α, only eligible for a minority of patients. In July 2020, the EMA granted Hepcludex conditional marketing authorization throughout the European Union. This first-in-class entry inhibitor offers the promise to prevent the spread in order to gain control and eventually participate in curing hepatitis B and D. Hepcludex is an example of how understanding the viral lifecycle can give rise to new therapy options. Sodium taurocholate co-transporting polypeptide, the virus receptor and the target of Hepcludex, and other targets of hepatitis D therapy currently researched are reviewed in this work. Farnesyltransferase inhibitors such as Lonafarnib, targeting another essential molecule in the HDV life cycle, represent a promising target for hepatitis D therapy. Farnesyltransferase attaches a farnesyl (isoprenyl) group to proteins carrying a C-terminal Ca1a2X (C: cysteine, a: aliphatic amino acid, X: C-terminal amino acid) motif like the large hepatitis D virus antigen. This modification enables the interaction of the HBV/HDV particle and the virus envelope proteins. Lonafarnib, which prevents this envelopment, has been tested in clinical trials. Targeting the lifecycle of the hepatitis B virus needs to be considered in hepatitis D therapy in order to cure a patient from both coexisting infections. Nucleic acid polymers target the hepatitis B lifecycle in a manner that is not yet understood. Understanding the possible targets of the hepatitis D virus therapy is inevitable for the improvement and development of a sufficient therapy that HDV patients are desperately in need of.
MeSH term(s)	Antiviral Agents/therapeutic use ; Cysteine ; Farnesyltranstransferase ; Hepatitis B/drug therapy ; Hepatitis B virus/metabolism ; Hepatitis D/drug therapy ; Hepatitis D/metabolism ; Hepatitis Delta Virus ; Humans ; Interferon-alpha/therapeutic use ; Nucleic Acids/therapeutic use ; Polymers/therapeutic use ; Receptors, Virus ; Taurocholic Acid ; Viral Envelope Proteins/metabolism
Chemical Substances	Antiviral Agents ; Interferon-alpha ; Nucleic Acids ; Polymers ; Receptors, Virus ; Viral Envelope Proteins ; Taurocholic Acid (5E090O0G3Z) ; Farnesyltranstransferase (EC 2.5.1.29) ; Cysteine (K848JZ4886)
Language	English
Publishing date	2022-09-16
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms231810817
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Bulevirtide als erster spezifischer Wirkstoff gegen Hepatitis-D-Virusinfektionen – Mechanismus und klinische Wirkung.

Nkongolo, Shirin / Hollnberger, Julius / Urban, Stephan

Bundesgesundheitsblatt, Gesundheitsforschung, Gesundheitsschutz

2022 Volume 65, Issue 2, Page(s) 254–263

Abstract: Blocking the cell entry of pathogens is a suitable approach to prevent new infections. However, the therapeutic use of entry inhibitors in chronically infected patients has had limited success. For the treatment of chronic hepatitis D virus (HDV) ... ...

Title translation	Bulevirtide as the first specific agent against hepatitis D virus infections-mechanism and clinical effect.
Abstract	Blocking the cell entry of pathogens is a suitable approach to prevent new infections. However, the therapeutic use of entry inhibitors in chronically infected patients has had limited success. For the treatment of chronic hepatitis D virus (HDV) infections, a promising agent based on this mode of action, Bulevirtide (BLV), was conditionally approved in July 2020. Previously, no drugs were available for HDV, and treatment relied on off-label use of interferon alpha/peginterferon alpha (IFNα/Peg-IFNα). In this review, we provide an overview of the basic mechanism of action of BLV and summarize the clinical data available to date.HDV infection manifests as a co-infection or superinfection of hepatitis B virus (HBV) infections and affects 4.5-15% of HBV patients worldwide. HDV utilizes the envelope proteins of HBV for dissemination. BLV acts by blocking the HBV/HDV receptor sodium taurocholate co-transporting polypeptide (NTCP), preventing HBV/HDV entry into hepatocytes. BLV lowers HDV serum RNA levels and normalizes alanine aminotransferase (ALT) levels in HBV/HDV-infected individuals. It has an excellent safety profile, even when administered at high doses (10 mg daily) for 48 weeks. In combination with Peg-IFNα, BLV shows synergistic effects on lowering serum HDV RNA, but also on hepatitis B surface antigen (HBsAg) levels. This resulted in a functional cure in a subset of patients when 2 mg BLV plus Peg-IFNα was administered. The mechanism of this likely immune-mediated elimination will be investigated in follow-up studies.
MeSH term(s)	Germany ; Hepatitis D/diagnosis ; Hepatitis D/drug therapy ; Hepatitis D, Chronic/drug therapy ; Hepatitis Delta Virus ; Humans ; Lipopeptides
Chemical Substances	Lipopeptides ; bulevirtide
Language	German
Publishing date	2022-01-13
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	1461973-8
ISSN	1437-1588 ; 1436-9990
ISSN (online)	1437-1588
ISSN	1436-9990
DOI	10.1007/s00103-022-03486-2
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Un I Zs.525: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Interplay between Hepatitis D Virus and the Interferon Response.

Zhang, Zhenfeng / Urban, Stephan

Viruses

2020 Volume 12, Issue 11

Abstract: Chronic hepatitis D (CHD) is the most severe form of viral hepatitis, with rapid progression of liver-related diseases and high rates of development of hepatocellular carcinoma. The causative agent, hepatitis D virus (HDV), contains a small ( ... ...

Abstract	Chronic hepatitis D (CHD) is the most severe form of viral hepatitis, with rapid progression of liver-related diseases and high rates of development of hepatocellular carcinoma. The causative agent, hepatitis D virus (HDV), contains a small (approximately 1.7 kb) highly self-pairing single-strand circular RNA genome that assembles with the HDV antigen to form a ribonucleoprotein (RNP) complex. HDV depends on hepatitis B virus (HBV) envelope proteins for envelopment and de novo hepatocyte entry; however, its intracellular RNA replication is autonomous. In addition, HDV can amplify HBV independently through cell division. Cellular innate immune responses, mainly interferon (IFN) response, are crucial for controlling invading viruses, while viruses counteract these responses to favor their propagation. In contrast to HBV, HDV activates profound IFN response through the melanoma differentiation antigen 5 (MDA5) pathway. This cellular response efficiently suppresses cell-division-mediated HDV spread and, to some extent, early stages of HDV de novo infection, but only marginally impairs RNA replication in resting hepatocytes. In this review, we summarize the current knowledge on HDV structure, replication, and persistence and subsequently focus on the interplay between HDV and IFN response, including IFN activation, sensing, antiviral effects, and viral countermeasures. Finally, we discuss crosstalk with HBV.
MeSH term(s)	Animals ; Hepatitis B virus/metabolism ; Hepatitis D, Chronic/immunology ; Hepatitis D, Chronic/virology ; Hepatitis Delta Virus/genetics ; Hepatitis Delta Virus/immunology ; Hepatitis Delta Virus/physiology ; Hepatocytes/virology ; Humans ; Immunity, Innate ; Interferon-Induced Helicase, IFIH1/immunology ; Interferons/immunology ; Mice ; Virus Replication/immunology
Chemical Substances	Interferons (9008-11-1) ; IFIH1 protein, human (EC 3.6.1.-) ; Interferon-Induced Helicase, IFIH1 (EC 3.6.4.13)
Language	English
Publishing date	2020-11-20
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v12111334
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: New insights into HDV persistence: The role of interferon response and implications for upcoming novel therapies.

Zhang, Zhenfeng / Urban, Stephan

Journal of hepatology

2020 Volume 74, Issue 3, Page(s) 686–699

Abstract: Chronic hepatitis D (CHD), a global health problem, manifests as the most severe form of viral hepatitis. The causative agent, HDV, is the smallest known human virus; it replicates its circular single-stranded RNA genome in the nucleus of hepatocytes. ... ...

Abstract	Chronic hepatitis D (CHD), a global health problem, manifests as the most severe form of viral hepatitis. The causative agent, HDV, is the smallest known human virus; it replicates its circular single-stranded RNA genome in the nucleus of hepatocytes. HDV requires HBV-encoded envelope proteins for dissemination and de novo cell entry. However, HDV can also spread through cell division. Following entry into hepatocytes, replicative intermediates of HDV RNA are sensed by the pattern recognition receptor MDA5 (melanoma differentiation antigen 5) resulting in interferon (IFN)-β/λ induction. This IFN response strongly suppresses cell division-mediated spread of HDV genomes, however, it only marginally affects HDV RNA replication in already infected, resting hepatocytes. Monotherapy with IFN-α/λ shows efficacy but rarely results in HDV clearance. Recent molecular insights into key determinants of HDV persistence and the accelerated development of specifically acting antivirals that interfere with the replication cycle have revealed promising new therapeutic perspectives. In this review, we briefly summarise our knowledge on replication/persistence of HDV, the newly discovered HDV-like agents, and the interplay of HDV with the IFN response and its consequences for persistence. Finally, we discuss the possible role of IFNs in combination with upcoming therapies aimed at HDV cure.
MeSH term(s)	Animals ; Antiviral Agents/pharmacology ; Antiviral Agents/therapeutic use ; Cell Division/drug effects ; Hepatitis B/complications ; Hepatitis B/virology ; Hepatitis B virus/metabolism ; Hepatitis D, Chronic/complications ; Hepatitis D, Chronic/drug therapy ; Hepatitis D, Chronic/immunology ; Hepatitis D, Chronic/virology ; Hepatitis Delta Virus/genetics ; Hepatitis Delta Virus/metabolism ; Hepatocytes/metabolism ; Hepatocytes/virology ; Humans ; Immunity, Innate ; Interferon-alpha/metabolism ; Interferon-beta/metabolism ; Treatment Outcome ; Virus Replication/drug effects
Chemical Substances	Antiviral Agents ; Interferon-alpha ; Interferon-beta (77238-31-4)
Language	English
Publishing date	2020-12-01
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/j.jhep.2020.11.032
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 2027: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Interplay between Hepatitis D Virus and the Interferon Response

Zhang, Zhenfeng / Urban, Stephan

Viruses. 2020 Nov. 20, v. 12, no. 11

2020

Abstract	Chronic hepatitis D (CHD) is the most severe form of viral hepatitis, with rapid progression of liver-related diseases and high rates of development of hepatocellular carcinoma. The causative agent, hepatitis D virus (HDV), contains a small (approximately 1.7 kb) highly self-pairing single-strand circular RNA genome that assembles with the HDV antigen to form a ribonucleoprotein (RNP) complex. HDV depends on hepatitis B virus (HBV) envelope proteins for envelopment and de novo hepatocyte entry; however, its intracellular RNA replication is autonomous. In addition, HDV can amplify HBV independently through cell division. Cellular innate immune responses, mainly interferon (IFN) response, are crucial for controlling invading viruses, while viruses counteract these responses to favor their propagation. In contrast to HBV, HDV activates profound IFN response through the melanoma differentiation antigen 5 (MDA5) pathway. This cellular response efficiently suppresses cell-division-mediated HDV spread and, to some extent, early stages of HDV de novo infection, but only marginally impairs RNA replication in resting hepatocytes. In this review, we summarize the current knowledge on HDV structure, replication, and persistence and subsequently focus on the interplay between HDV and IFN response, including IFN activation, sensing, antiviral effects, and viral countermeasures. Finally, we discuss crosstalk with HBV.
Keywords	Hepatitis B virus ; Hepatitis delta virus ; RNA replication ; antigens ; antiviral properties ; cell division ; chronic hepatitis D ; circular RNA ; etiological agents ; genome ; hepatocytes ; hepatoma ; innate immunity ; interferons ; melanoma ; ribonucleoproteins ; viruses
Language	English
Dates of publication	2020-1120
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2516098-9
ISSN	1999-4915
ISSN	1999-4915
DOI	10.3390/v12111334
Database	NAL-Catalogue (AGRICOLA)

Order via subito

Article ; Online: Effect of variants in LGP2 on MDA5-mediated activation of interferon response and suppression of hepatitis D virus replication.

Gillich, Nadine / Zhang, Zhenfeng / Binder, Marco / Urban, Stephan / Bartenschlager, Ralf

Journal of hepatology

2022 Volume 78, Issue 1, Page(s) 78–89

Abstract: Background & aims: Retinoic acid inducible gene I (RIG-I)-like receptors (RLRs), including RIG-I, melanoma differentiation-associated protein 5 (MDA5), and laboratory of genetics and physiology 2 (LGP2), sense viral RNA to induce the antiviral ... ...

Abstract	Background & aims: Retinoic acid inducible gene I (RIG-I)-like receptors (RLRs), including RIG-I, melanoma differentiation-associated protein 5 (MDA5), and laboratory of genetics and physiology 2 (LGP2), sense viral RNA to induce the antiviral interferon (IFN) response. LGP2, unable to activate the IFN response itself, modulates RIG-I and MDA5 signalling. HDV, a small RNA virus causing the most severe form of viral hepatitis, is sensed by MDA5. The mechanism underlying IFN induction and its effect on HDV replication is unclear. Here, we aimed to unveil the role of LGP2 and clinically relevant variants thereof in these processes. Methods: RLRs were depleted in HDV susceptible HepaRG Results: LGP2 is essential for the MDA5-mediated IFN response induced upon HDV infection. This induction requires both RNA binding and ATPase activities of LGP2. The IFN response only moderately reduced HDV replication in resting cells but profoundly suppressed cell division-mediated HDV spread. An LGP2 variant (Q425R), predominating in Africans who develop less severe chronic hepatitis D, mediated detectably higher basal and faster HDV-induced IFN response as well as stronger HDV suppression. Mechanistically, LGP2 RNA binding was a prerequisite for the formation of stable MDA5-RNA complexes. MDA5 binding to RNA was enhanced by the Q425R LGP2 variant. Conclusions: LGP2 is essential to mount an antiviral IFN response induced by HDV and stabilises MDA5-RNA interaction required for downstream signalling. The natural Q425R LGP2 is a gain-of-function variant and might contribute to an attenuated course of hepatitis D. Impact and implications: HDV is the causative pathogen of chronic hepatitis D, a severe form of viral hepatitis that can lead to cirrhosis and hepatocellular carcinoma. Upon infection, the human immune system senses HDV and mounts an antiviral interferon (IFN) response. Here, we demonstrate that the immune sensor LGP2 cooperates with MDA5 to mount an IFN response that represses HDV replication. We mapped LGP2 determinants required for IFN system activation and characterised several natural genetic variants of LGP2. One of them reported to predominate in sub-Saharan Africans can accelerate HDV-induced IFN responses, arguing that genetic determinants, possibly including LGP2, might contribute to slower disease progression in this population. Our results will hopefully prompt further studies on genetic variations in LGP2 and other components of the innate immune sensing system, including assessments of their possible impact on the course of viral infection.
MeSH term(s)	Humans ; Antiviral Agents ; Hepatitis D, Chronic ; Hepatitis Delta Virus/genetics ; Immunity, Innate ; Interferon-Induced Helicase, IFIH1/genetics ; Interferon-Induced Helicase, IFIH1/metabolism ; Interferons ; RNA Helicases/genetics ; RNA Helicases/metabolism ; RNA, Viral/genetics ; RNA, Viral/metabolism ; Virus Replication
Chemical Substances	Antiviral Agents ; Interferon-Induced Helicase, IFIH1 (EC 3.6.4.13) ; Interferons (9008-11-1) ; RNA Helicases (EC 3.6.4.13) ; RNA, Viral ; IFIH1 protein, human (EC 3.6.1.-) ; DHX58 protein, human (EC 2.7.7.-)
Language	English
Publishing date	2022-09-22
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/j.jhep.2022.08.041
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 2027: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Quantification of Hepatitis B Virus Covalently Closed Circular DNA in Infected Cell Culture Models by Quantitative PCR.

Qu, Bingqian / Urban, Stephan

Bio-protocol

2019 Volume 9, Issue 7, Page(s) e3202

Abstract: Persistence of the human hepatitis B virus (HBV) requires the maintenance of covalently closed circular (ccc)DNA, the episomal genome reservoir in nuclei of infected hepatocytes. cccDNA elimination is a major aim in future curative therapies currently ... ...

Abstract	Persistence of the human hepatitis B virus (HBV) requires the maintenance of covalently closed circular (ccc)DNA, the episomal genome reservoir in nuclei of infected hepatocytes. cccDNA elimination is a major aim in future curative therapies currently under development. In cell culture based
Language	English
Publishing date	2019-04-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	2833269-6
ISSN	2331-8325 ; 2331-8325
ISSN (online)	2331-8325
ISSN	2331-8325
DOI	10.21769/BioProtoc.3202
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: A Sensitive and Specific PCR-based Assay to Quantify Hepatitis B Virus Covalently Closed Circular (ccc) DNA while Preserving Cellular DNA.

Zehnder, Benno / Urban, Stephan / Tu, Thomas

Bio-protocol

2021 Volume 11, Issue 8, Page(s) e3986

Abstract: Hepatitis B virus (HBV) is the major cause of liver diseases and liver cancer worldwide. After infecting hepatocytes, the virus establishes a stable episome (covalently closed circular DNA, or cccDNA) that serves as the template for all viral transcripts. ...

Abstract	Hepatitis B virus (HBV) is the major cause of liver diseases and liver cancer worldwide. After infecting hepatocytes, the virus establishes a stable episome (covalently closed circular DNA, or cccDNA) that serves as the template for all viral transcripts. Specific and accurate quantification of cccDNA is difficult because infected cells contain abundant replicative intermediates of HBV DNA that share overlapping sequences but arranged in slightly different forms. HBV cccDNA can be detected by Southern blot or qPCR methods which involve enzymatic digestion. These assays are laborious, have limited sensitivity, or require degradation of cellular DNA (which precludes simple normalization). The method described in this protocol, cccDNA inversion quantitative (cinq)PCR, instead uses a series of restriction enzyme-mediated hydrolysis and ligation reactions that convert cccDNA into an inverted linear amplicon, which is not amplified or detected from other forms of HBV DNA. Importantly, cellular DNA remains quantifiable during sample preparation, allowing normalization and markedly improving precision. Further, a second linear fragment (derived from enzymatic digestion of a separate region of the HBV DNA genome and is present in all forms of HBV DNA) can be used to simultaneously quantify total HBV levels. Graphic abstract:
Language	English
Publishing date	2021-04-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2833269-6
ISSN	2331-8325 ; 2331-8325
ISSN (online)	2331-8325
ISSN	2331-8325
DOI	10.21769/BioProtoc.3986
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

To top

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito