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Article ; Online: Lytic Replication and Reactivation from B Cells Is Not Required for Establishing or Maintaining Gammaherpesvirus Latency

Gupta, Arundhati / Owens, Shana M / Oldenburg, Darby G / White, Douglas W / Forrest, J Craig

2022 Volume 96, Issue 12, Page(s) e0069022

Abstract: Gammaherpesviruses (GHVs) are lymphotropic tumor viruses with a biphasic infectious cycle. Lytic replication at the primary site of infection is necessary for GHVs to spread throughout the host and establish latency in distal sites. Dissemination is ... ...

Abstract	Gammaherpesviruses (GHVs) are lymphotropic tumor viruses with a biphasic infectious cycle. Lytic replication at the primary site of infection is necessary for GHVs to spread throughout the host and establish latency in distal sites. Dissemination is mediated by infected B cells that traffic hematogenously from draining lymph nodes to peripheral lymphoid organs, such as the spleen. B cells serve as the major reservoir for viral latency, and it is hypothesized that periodic reactivation from latently infected B cells contributes to maintaining long-term chronic infection. While fundamentally important to an understanding of GHV biology, aspects of B cell infection in latency establishment and maintenance are incompletely defined, especially roles for lytic replication and reactivation in this cell type. To address this knowledge gap and overcome limitations of replication-defective viruses, we generated a recombinant murine gammaherpesvirus 68 (MHV68) in which
MeSH term(s)	Animals ; B-Lymphocytes/virology ; Gammaherpesvirinae/genetics ; Gammaherpesvirinae/physiology ; Herpesviridae Infections/virology ; Immediate-Early Proteins/genetics ; Mice ; Mice, Inbred C57BL ; Virus Activation ; Virus Latency ; Virus Replication
Chemical Substances	Immediate-Early Proteins
Language	English
Publishing date	2022-06-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/jvi.00690-22
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Uracil-DNA glycosylase of murine gammaherpesvirus 68 binds cognate viral replication factors independently of its catalytic residues.

Smith, Kyle R / Paul, Somnath / Dong, Qiwen / Anannya, Orchi / Oldenburg, Darby G / Forrest, J Craig / McBride, Kevin M / Krug, Laurie T

mSphere

2023 Volume 8, Issue 5, Page(s) e0027823

Abstract: Herpesviruses are large double-stranded DNA viruses that encode core replication proteins and accessory factors involved in nucleotide metabolism and DNA repair. Mammalian uracil-DNA glycosylases (UNG) excise deleterious uracil residues from their ... ...

Abstract	Herpesviruses are large double-stranded DNA viruses that encode core replication proteins and accessory factors involved in nucleotide metabolism and DNA repair. Mammalian uracil-DNA glycosylases (UNG) excise deleterious uracil residues from their genomic DNA. Each herpesvirus UNG studied to date has demonstrated conservation of the enzymatic function to excise uracil residues from DNA. We previously reported that a murine gammaherpesvirus (MHV68) with a stop codon in
MeSH term(s)	Animals ; Mice ; Uracil-DNA Glycosidase/genetics ; Uracil-DNA Glycosidase/metabolism ; Virus Replication ; DNA Replication ; DNA, Viral/genetics ; Rhadinovirus/genetics ; Rhadinovirus/metabolism ; Gammaherpesvirinae/genetics ; DNA-Directed DNA Polymerase/genetics ; DNA-Directed DNA Polymerase/metabolism ; Uracil ; Mammals
Chemical Substances	Uracil-DNA Glycosidase (EC 3.2.2.-) ; DNA, Viral ; DNA-Directed DNA Polymerase (EC 2.7.7.7) ; Uracil (56HH86ZVCT)
Language	English
Publishing date	2023-09-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Intramural ; Research Support, N.I.H., Extramural
ISSN	2379-5042
ISSN (online)	2379-5042
DOI	10.1128/msphere.00278-23
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Uracil-DNA Glycosylase of Murine Gammaherpesvirus 68 Binds Cognate Viral Replication Factors Independently of its Catalytic Residues.

Smith, Kyle R / Paul, Somnath / Dong, Qiwen / Anannya, Orchi / Oldenburg, Darby G / Forrest, J Craig / McBride, Kevin M / Krug, Laurie T

bioRxiv : the preprint server for biology

2023

Abstract: Herpesviruses are large double-stranded DNA viruses that encode core replication proteins and accessory factors involved in nucleotide metabolism and DNA repair. Mammalian Uracil-DNA glycosylases (UNG) excise deleterious uracil residues from their ... ...

Abstract	Herpesviruses are large double-stranded DNA viruses that encode core replication proteins and accessory factors involved in nucleotide metabolism and DNA repair. Mammalian Uracil-DNA glycosylases (UNG) excise deleterious uracil residues from their genomic DNA. Each herpesvirus UNG studied to date has demonstrated conservation of the enzymatic function to excise uracil residues from DNA. We previously reported that a murine gammaherpesvirus (MHV68) with a stop codon in Importance: Gammaherpesviruses encode a uracil-DNA glycosylase (vUNG) that is presumed to excise uracil residues from viral genomes. We previously identified the vUNG enzymatic activity, but not the protein itself, as dispensable for gammaherpesvirus replication
Language	English
Publishing date	2023-05-19
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.05.19.541466
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Article ; Online: Deletion of Murine Gammaherpesvirus Gene

Owens, Shana M / Oldenburg, Darby G / White, Douglas W / Forrest, J Craig

Journal of virology

2020 Volume 95, Issue 1

Abstract: Gammaherpesviruses (GHVs) are DNA tumor viruses that establish lifelong, chronic infections in lymphocytes of humans and other mammals. GHV infections are associated with numerous cancers, especially in immunocompromised hosts. While it is known that ... ...

Abstract	Gammaherpesviruses (GHVs) are DNA tumor viruses that establish lifelong, chronic infections in lymphocytes of humans and other mammals. GHV infections are associated with numerous cancers, especially in immunocompromised hosts. While it is known that GHVs utilize host germinal center (GC) B cell responses during latency establishment, an understanding of how viral gene products function in specific B cell subsets to regulate this process is incomplete. Using murine gammaherpesvirus 68 (MHV68) as a small-animal model to define mechanisms of GHV pathogenesis
MeSH term(s)	Animals ; Antigens, CD19/metabolism ; B-Lymphocytes/immunology ; B-Lymphocytes/virology ; Cell Differentiation ; Cell Proliferation ; Cytidine Deaminase/immunology ; Germinal Center/immunology ; Germinal Center/virology ; Herpesviridae Infections/immunology ; Herpesviridae Infections/virology ; Lymphoid Tissue/immunology ; Lymphoid Tissue/virology ; Mice ; Rhadinovirus/genetics ; Rhadinovirus/metabolism ; Rhadinovirus/physiology ; Viral Proteins/genetics ; Viral Proteins/immunology ; Virus Activation ; Virus Latency
Chemical Substances	Antigens, CD19 ; CD19 antigen, mouse ; M2 protein, murine gammaherpesvirus 68 ; Viral Proteins ; Cytidine Deaminase (EC 3.5.4.5)
Language	English
Publishing date	2020-12-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.01933-20
Database	MEDical Literature Analysis and Retrieval System OnLINE

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ab Jg. 2022: Lesesaal (EG)

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Article: Replication-dead gammaherpesvirus vaccine protects against acute replication, reactivation from latency, and lethal challenge in mice.

Bland, Wesley A / Owens, Shana / McEvoy, Kyle / Hogan, Chad H / Boccuzzi, Luciarita / Kirillov, Varvara / Khairallah, Camille / Sheridan, Brian S / Forrest, J Craig / Krug, Laurie T

bioRxiv : the preprint server for biology

2023

Abstract: Gammaherpesviruses (GHVs) are oncogenic viruses that establish lifelong infections and are significant causes of human morbidity and mortality. While several vaccine strategies to limit GHV infection and disease are in development, there are no FDA- ... ...

Abstract	Gammaherpesviruses (GHVs) are oncogenic viruses that establish lifelong infections and are significant causes of human morbidity and mortality. While several vaccine strategies to limit GHV infection and disease are in development, there are no FDA-approved vaccines for human GHVs. As a new approach to gammaherpesvirus vaccination, we developed and tested a replication-dead virus (RDV) platform, using murine gammaherpesvirus 68 (MHV68), a well-established mouse model for gammaherpesvirus pathogenesis studies and preclinical therapeutic evaluations. We employed codon-shuffling-based complementation to generate revertant-free RDV lacking expression of the essential replication and transactivator protein (RTA) encoded by
Language	English
Publishing date	2023-09-26
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.09.26.559621
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Intrinsic p53 Activation Restricts Gammaherpesvirus-Driven Germinal Center B Cell Expansion during Latency Establishment.

Owens, Shana M / Sifford, Jeffrey M / Li, Gang / Murdock, Steven J / Salinas, Eduardo / Manzano, Mark / Ghosh, Debopam / Stumhofer, Jason S / Forrest, J Craig

bioRxiv : the preprint server for biology

2023

Abstract: Gammaherpesviruses (GHV) are DNA tumor viruses that establish lifelong latent infections in lymphocytes. For viruses such as Epstein-Barr virus (EBV) and murine gammaherpesvirus 68 (MHV68), this is accomplished through a viral gene-expression program ... ...

Abstract	Gammaherpesviruses (GHV) are DNA tumor viruses that establish lifelong latent infections in lymphocytes. For viruses such as Epstein-Barr virus (EBV) and murine gammaherpesvirus 68 (MHV68), this is accomplished through a viral gene-expression program that promotes cellular proliferation and differentiation, especially of germinal center (GC) B cells. Intrinsic host mechanisms that control virus-driven cellular expansion are incompletely defined. Using a small-animal model of GHV pathogenesis, we demonstrate Importance: Gammaherpesviruses cause lifelong infections of their hosts, commonly referred to as latency, that can lead to cancer. Latency establishment benefits from the functions of viral proteins that augment and amplify B cell activation, proliferation, and differentiation signals. In uninfected cells, off-schedule cellular differentiation would typically trigger anti-proliferative responses by effector proteins known as tumor suppressors. However, tumor suppressor responses to gammaherpesvirus manipulation of cellular processes remain understudied, especially those that occur during latency establishment in a living organism. Here we identify p53, a tumor suppressor commonly mutated in cancer, as a host factor that limits virus-driven B cell proliferation and differentiation, and thus, viral colonization of a host. We demonstrate that p53 activation occurs in response to viral latency proteins that induce B cell activation. This work informs a gap in our understanding of intrinsic cellular defense mechanisms that restrict lifelong GHV infection.
Language	English
Publishing date	2023-11-01
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.10.31.563188
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Murine Gammaherpesvirus 68: A Small Animal Model for Gammaherpesvirus-Associated Diseases.

Dong, Sihan / Forrest, J Craig / Liang, Xiaozhen

Advances in experimental medicine and biology

2017 Volume 1018, Page(s) 225–236

Abstract: Murine gammaherpesvirus 68 (MHV68) is a naturally occurring pathogen of murid rodents that is genetically related to the human gammaherpesviruses Epstein-Barr virus (EBV) and Kaposi sarcoma-associated herpesvirus (KSHV). Viral, immunologic, and disease ... ...

Abstract	Murine gammaherpesvirus 68 (MHV68) is a naturally occurring pathogen of murid rodents that is genetically related to the human gammaherpesviruses Epstein-Barr virus (EBV) and Kaposi sarcoma-associated herpesvirus (KSHV). Viral, immunologic, and disease parameters following experimental infection of laboratory mice with MHV68 closely resemble what occurs during primary EBV infection of humans, which suggests that MHV68 infection of mice offers a small animal model to study in general the pathogenesis of gammaherpesvirus infections. Diseases elicited by MHV68 infection include lymphoproliferative diseases, idiopathic pulmonary fibrosis, and autoimmune diseases, ailments also associated with EBV infection of humans. Furthermore, MHV68 infection also is linked to the development of vasculitis, encephalomyelitis, and other disorders that resemble pathologies with viral and nonviral etiologies in humans. This review aims to provide an overview of MHV68-associated diseases in infected mice that may provide a model for understanding basic mechanisms by which similar diseases in humans occur and can be treated.
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-981-10-5765-6_14
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Development of ACE2 autoantibodies after SARS-CoV-2 infection.

Arthur, John M / Forrest, J Craig / Boehme, Karl W / Kennedy, Joshua L / Owens, Shana / Herzog, Christian / Liu, Juan / Harville, Terry O

PloS one

2021 Volume 16, Issue 9, Page(s) e0257016

Abstract: Background: Activation of the immune system is implicated in the Post-Acute Sequelae after SARS-CoV-2 infection (PASC) but the mechanisms remain unknown. Angiotensin-converting enzyme 2 (ACE2) cleaves angiotensin II (Ang II) resulting in decreased ... ...

Abstract	Background: Activation of the immune system is implicated in the Post-Acute Sequelae after SARS-CoV-2 infection (PASC) but the mechanisms remain unknown. Angiotensin-converting enzyme 2 (ACE2) cleaves angiotensin II (Ang II) resulting in decreased activation of the AT1 receptor and decreased immune system activation. We hypothesized that autoantibodies against ACE2 may develop after SARS-CoV-2 infection, as anti-idiotypic antibodies to anti-spike protein antibodies. Methods and findings: We tested plasma or serum for ACE2 antibodies in 67 patients with known SARS-CoV-2 infection and 13 with no history of infection. None of the 13 patients without history of SARS-CoV-2 infection and 1 of the 20 outpatients that had a positive PCR test for SARS-CoV-2 had levels of ACE2 antibodies above the cutoff threshold. In contrast, 26/32 (81%) in the convalescent group and 14/15 (93%) of patients acutely hospitalized had detectable ACE2 antibodies. Plasma from patients with antibodies against ACE2 had less soluble ACE2 activity in plasma but similar amounts of ACE2 protein compared to patients without ACE2 antibodies. We measured the capacity of the samples to inhibit ACE2 enzyme activity. Addition of plasma from patients with ACE2 antibodies led to decreased activity of an exogenous preparation of ACE2 compared to patients that did not have antibodies. Conclusions: Many patients with a history of SARS-CoV-2 infection have antibodies specific for ACE2. Patients with ACE2 antibodies have lower activity of soluble ACE2 in plasma. Plasma from these patients also inhibits exogenous ACE2 activity. These findings are consistent with the hypothesis that ACE2 antibodies develop after SARS-CoV-2 infection and decrease ACE2 activity. This could lead to an increase in the abundance of Ang II, which causes a proinflammatory state that triggers symptoms of PASC.
MeSH term(s)	Angiotensin II/blood ; Angiotensin II/immunology ; Angiotensin-Converting Enzyme 2/genetics ; Autoantibodies/blood ; Autoantibodies/immunology ; Autoantibodies/isolation & purification ; COVID-19/blood ; COVID-19/immunology ; COVID-19/virology ; Female ; Humans ; Male ; Peptidyl-Dipeptidase A/blood ; Receptor, Angiotensin, Type 1/blood ; Receptor, Angiotensin, Type 1/genetics ; Receptor, Angiotensin, Type 1/immunology ; Renin-Angiotensin System/genetics ; Renin-Angiotensin System/immunology ; SARS-CoV-2/genetics ; SARS-CoV-2/immunology ; SARS-CoV-2/isolation & purification ; Spike Glycoprotein, Coronavirus/blood ; Spike Glycoprotein, Coronavirus/immunology ; Spike Glycoprotein, Coronavirus/isolation & purification
Chemical Substances	Autoantibodies ; Receptor, Angiotensin, Type 1 ; Spike Glycoprotein, Coronavirus ; Angiotensin II (11128-99-7) ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; ACE2 protein, human (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
Language	English
Publishing date	2021-09-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0257016
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Article ; Online: Multifaceted roles for STAT3 in gammaherpesvirus latency revealed through

Hogan, Chad H / Owens, Shana M / Reynoso, Glennys V / Liao, Yifei / Meyer, Thomas J / Zelazowska, Monika A / Liu, Bin / Li, Xiaofan / Grosskopf, Anna K / Khairallah, Camille / Kirillov, Varvara / Reich, Nancy C / Sheridan, Brian S / McBride, Kevin M / Gewurz, Benjamin E / Hickman, Heather D / Forrest, J Craig / Krug, Laurie T

mBio

2024 Volume 15, Issue 2, Page(s) e0299823

Abstract: Cancers associated with the oncogenic gammaherpesviruses, Epstein-Barr virus and Kaposi sarcoma herpesvirus, are notable for their constitutive activation of the transcription factor signal transducer and activator of transcription 3 (STAT3). To better ... ...

Abstract	Cancers associated with the oncogenic gammaherpesviruses, Epstein-Barr virus and Kaposi sarcoma herpesvirus, are notable for their constitutive activation of the transcription factor signal transducer and activator of transcription 3 (STAT3). To better understand the role of STAT3 during gammaherpesvirus latency and the B cell response to infection, we used the model pathogen murine gammaherpesvirus 68 (MHV68). Genetic deletion of STAT3 in B cells of
MeSH term(s)	Animals ; Humans ; Mice ; Epstein-Barr Virus Infections ; Gammaherpesvirinae/genetics ; Herpesviridae Infections ; Herpesvirus 4, Human/genetics ; Herpesvirus 4, Human/metabolism ; Herpesvirus 8, Human/metabolism ; Mice, Inbred C57BL ; Rhadinovirus/genetics ; Sarcoma, Kaposi ; STAT3 Transcription Factor/genetics ; STAT3 Transcription Factor/metabolism ; Virus Latency/genetics
Chemical Substances	STAT3 protein, human ; STAT3 Transcription Factor ; Stat3 protein, mouse
Language	English
Publishing date	2024-01-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mbio.02998-23
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: IRF4 promotes Epstein-Barr virus activation in Burkitt's lymphoma cells.

Gao, Ying / Wang, Liu / Lei, Zhangmengxue / Li, Jie / Forrest, J Craig / Liang, Xiaozhen

The Journal of general virology

2019 Volume 100, Issue 5, Page(s) 851–862

Abstract: Epstein-Barr virus (EBV) establishes a life-long latency in memory B cells, whereas plasma cell differentiation is linked to EBV lytic reactivation from latently infected B cells. EBV lytic replication is mediated by the two immediate-early switch ... ...

Abstract	Epstein-Barr virus (EBV) establishes a life-long latency in memory B cells, whereas plasma cell differentiation is linked to EBV lytic reactivation from latently infected B cells. EBV lytic replication is mediated by the two immediate-early switch proteins Zta and RTA. Both plasma cell transcription factors XBP-1 and Blimp-1 have been shown to enable the triggering of EBV lytic reactivation by activating the transcription of Zta or RTA. Here we show that interferon regulatory factor 4 (IRF4), another plasma cell transcription factor that is either not expressed or expressed at a low level in EBV-positive Burkitt's lymphoma (BL) cells, can activate the promoters of EBV Zta and RTA, but is not sufficient to elicit EBV lytic reactivation in latently infected BL cells. However, ectopic IRF4 expression can augment EBV lytic gene expression induced by anti-immunoglobulin (anti-Ig) or sodium butyrate treatment in all tested lymphoma cells, whereas IRF4 knockout in Raji cells, the only BL cell line with detectable endogenous IRF4 expression, abolishes EBV lytic gene expression induced by anti-Ig, and this is accompanied by the reduction of Blimp-1 expression, whose overexpression, in turn, can rescue EBV lytic gene expression in IRF4 knockout Raji cells. Furthermore, IRF4 knockout impairs B cell receptor (BCR) signalling activation, which is required for BCR-mediated EBV reactivation. Altogether, these results demonstrate that IRF4 facilitates EBV lytic reactivation in BL cells, which involves the regulation of Blimp-1 expression and BCR signalling pathways.
MeSH term(s)	B-Lymphocytes/virology ; Burkitt Lymphoma/virology ; Cell Line, Tumor ; Epstein-Barr Virus Infections/virology ; Gene Expression Regulation, Viral/genetics ; Herpesvirus 4, Human/genetics ; Humans ; Interferon Regulatory Factors/genetics ; Positive Regulatory Domain I-Binding Factor 1/genetics ; Promoter Regions, Genetic/genetics ; Signal Transduction/genetics ; Viral Proteins/genetics ; Virus Activation/genetics ; Virus Latency/genetics
Chemical Substances	Interferon Regulatory Factors ; Viral Proteins ; interferon regulatory factor-4 ; Positive Regulatory Domain I-Binding Factor 1 (EC 2.1.1.-)
Language	English
Publishing date	2019-03-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	219316-4
ISSN	1465-2099 ; 0022-1317
ISSN (online)	1465-2099
ISSN	0022-1317
DOI	10.1099/jgv.0.001249
Database	MEDical Literature Analysis and Retrieval System OnLINE

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