LIVIVO - Search results -

Search results

Result 1 - 9 of total 9

Search options

Article: Highly Pathogenic H5N1 Influenza A Virus Spreads Efficiently in Human Primary Monocyte-Derived Macrophages and Dendritic Cells.

Westenius, Veera / Mäkelä, Sanna M / Julkunen, Ilkka / Österlund, Pamela

2018 Volume 9, Page(s) 1664

Abstract: Influenza A viruses cause recurrent epidemics and occasional global pandemics. Wild birds are the natural reservoir of influenza A virus from where the virus can be transmitted to poultry or to mammals including humans. Mortality among humans in the ... ...

Abstract	Influenza A viruses cause recurrent epidemics and occasional global pandemics. Wild birds are the natural reservoir of influenza A virus from where the virus can be transmitted to poultry or to mammals including humans. Mortality among humans in the highly pathogenic avian influenza H5N1 virus infection is even 60%. Despite intense research, there are still open questions in the pathogenicity of the H5N1 virus in humans. To characterize the H5N1 virus infection in human monocyte-derived macrophages (Mɸs) and dendritic cells (DCs), we used human isolates of highly pathogenic H5N1/2004 and H5N1/1997 and low pathogenic H7N9/2013 avian influenza viruses in comparison with a seasonal H3N2/1989 virus. We noticed that the H5N1 viruses have an overwhelming ability to replicate and spread in primary human immune cell cultures, and even the addition of trypsin did not equalize the infectivity of H7N9 or H3N2 viruses to the level seen with H5N1 virus. H5N1 virus stocks contained more often propagation-competent viruses than the H7N9 or H3N2 viruses. The data also showed that human DCs and Mɸs maintain 1,000- and 10,000-fold increase in the production of infectious H5N1 virus, respectively. Both analyzed highly pathogenic H5N1 viruses showed multi-cycle infection in primary human DCs and Mɸs, whereas the H3N2 and H7N9 viruses were incapable of spreading in immune cells. Interestingly, H5N1 virus was able to spread extremely efficiently despite the strong induction of antiviral interferon gene expression, which may in part explain the high pathogenicity of H5N1 virus infection in humans.
Language	English
Publishing date	2018
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2018.01664
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: Zika Virus Non-Structural Protein NS5 Inhibits the RIG-I Pathway and Interferon Lambda 1 Promoter Activation by Targeting IKK Epsilon.

Lundberg, Rickard / Melén, Krister / Westenius, Veera / Jiang, Miao / Österlund, Pamela / Khan, Hira / Vapalahti, Olli / Julkunen, Ilkka / Kakkola, Laura

Viruses

2019 Volume 11, Issue 11

Abstract: The Zika virus (ZIKV) is a member of ... ...

Abstract	The Zika virus (ZIKV) is a member of the
MeSH term(s)	Cell Line ; DEAD Box Protein 58/metabolism ; Humans ; I-kappa B Kinase/metabolism ; Interferon Regulatory Factor-3/metabolism ; Interferon-beta/genetics ; Interferon-beta/metabolism ; Interferons/genetics ; Interferons/metabolism ; Interleukins/genetics ; Interleukins/metabolism ; NF-kappa B/metabolism ; Phosphorylation ; Promoter Regions, Genetic ; Protein Binding ; Receptors, Immunologic ; Signal Transduction ; Viral Nonstructural Proteins/genetics ; Viral Nonstructural Proteins/metabolism ; Zika Virus/metabolism ; Zika Virus/physiology ; Zika Virus Infection/metabolism ; Zika Virus Infection/virology
Chemical Substances	interferon-lambda, human ; IRF3 protein, human ; Interferon Regulatory Factor-3 ; Interleukins ; NF-kappa B ; NS5 protein, flavivirus ; Receptors, Immunologic ; Viral Nonstructural Proteins ; Interferon-beta (77238-31-4) ; Interferons (9008-11-1) ; I-kappa B Kinase (EC 2.7.11.10) ; IKBKE protein, human (EC 2.7.11.10) ; RIGI protein, human (EC 3.6.1.-) ; DEAD Box Protein 58 (EC 3.6.4.13)
Keywords	covid19
Language	English
Publishing date	2019-11-04
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v11111024
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Efficient Inhibition of Avian and Seasonal Influenza A Viruses by a Virus-Specific Dicer-Substrate Small Interfering RNA Swarm in Human Monocyte-Derived Macrophages and Dendritic Cells.

Jiang, Miao / Österlund, Pamela / Westenius, Veera / Guo, Deyin / Poranen, Minna M / Bamford, Dennis H / Julkunen, Ilkka

Journal of virology

2019 Volume 93, Issue 4

Abstract: Influenza A viruses (IAVs) are viral pathogens that cause epidemics and occasional pandemics of significant mortality. The generation of efficacious vaccines and antiviral drugs remains a challenge due to the rapid appearance of new influenza virus types ...

Abstract	Influenza A viruses (IAVs) are viral pathogens that cause epidemics and occasional pandemics of significant mortality. The generation of efficacious vaccines and antiviral drugs remains a challenge due to the rapid appearance of new influenza virus types and antigenic variants. Consequently, novel strategies for the prevention and treatment of IAV infections are needed, given the limitations of the presently available antivirals. Here, we used enzymatically produced IAV-specific double-stranded RNA (dsRNA) molecules and
MeSH term(s)	Animals ; Antiviral Agents/pharmacology ; Birds ; Cell Line ; DEAD-box RNA Helicases ; Dendritic Cells/drug effects ; Dendritic Cells/virology ; Dogs ; Host-Pathogen Interactions/drug effects ; Humans ; Influenza A Virus, H5N1 Subtype/genetics ; Influenza A Virus, H7N9 Subtype/genetics ; Influenza A virus/genetics ; Influenza in Birds/genetics ; Influenza in Birds/virology ; Influenza, Human/genetics ; Influenza, Human/virology ; Interferons/pharmacology ; Macrophages/drug effects ; Macrophages/virology ; Madin Darby Canine Kidney Cells ; Primary Cell Culture ; RNA, Small Interfering/genetics ; RNA, Small Interfering/pharmacology ; Ribonuclease III ; Virus Replication/drug effects
Chemical Substances	Antiviral Agents ; RNA, Small Interfering ; Interferons (9008-11-1) ; DICER1 protein, human (EC 3.1.26.3) ; Ribonuclease III (EC 3.1.26.3) ; DEAD-box RNA Helicases (EC 3.6.4.13)
Keywords	covid19
Language	English
Publishing date	2019-02-05
Publishing country	United States
Document type	Journal Article ; 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.01916-18
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 609: 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: Zika Virus Non-Structural Protein NS5 Inhibits the RIG-I Pathway and Interferon Lambda 1 Promoter Activation by Targeting IKK Epsilon

Lundberg, Rickard / Melén, Krister / Westenius, Veera / Jiang, Miao / Österlund, Pamela / Khan, Hira / Vapalahti, Olli / Julkunen, Ilkka / Kakkola, Laura

Viruses. 2019 Nov. 04, v. 11, no. 11

2019

Abstract: The Zika virus (ZIKV) is a member of the Flaviviridae family and an important human pathogen. Most pathogenic viruses encode proteins that interfere with the activation of host innate immune responses. Like other flaviviruses, ZIKV interferes with the ... ...

Abstract	The Zika virus (ZIKV) is a member of the Flaviviridae family and an important human pathogen. Most pathogenic viruses encode proteins that interfere with the activation of host innate immune responses. Like other flaviviruses, ZIKV interferes with the expression of interferon (IFN) genes and inhibits IFN-induced antiviral responses. ZIKV infects through epithelial barriers where IFN-λ1 is an important antiviral molecule. In this study, we analyzed the effects of ZIKV proteins on the activation of IFN-λ1 promoter. All ZIKV proteins were cloned and transiently expressed. ZIKV NS5, but no other ZIKV protein, was able to interfere with the RIG-I signaling pathway. This inhibition took place upstream of interferon regulatory factor 3 (IRF3) resulting in reduced phosphorylation of IRF3 and reduced activation of IFN-λ1 promoter. Furthermore, we showed that ZIKV NS5 interacts with the protein kinase IKKε, which is likely critical to the observed inhibition of phosphorylation of IRF3.
Keywords	Zika virus ; animal pathogens ; epithelium ; genes ; innate immunity ; interferon regulatory factor-3 ; interferons ; phosphorylation ; protein kinases ; signal transduction ; viral nonstructural proteins ; viruses ; covid19
Language	English
Dates of publication	2019-1104
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2516098-9
ISSN	1999-4915
ISSN	1999-4915
DOI	10.3390/v11111024
Database	NAL-Catalogue (AGRICOLA)

Order via subito

Article ; Online: Asian and African lineage Zika viruses show differential replication and innate immune responses in human dendritic cells and macrophages.

Österlund, Pamela / Jiang, Miao / Westenius, Veera / Kuivanen, Suvi / Järvi, Riia / Kakkola, Laura / Lundberg, Rickard / Melén, Krister / Korva, Miša / Avšič-Županc, Tatjana / Vapalahti, Olli / Julkunen, Ilkka

Scientific reports

2019 Volume 9, Issue 1, Page(s) 15710

Abstract: Zika virus (ZIKV) infections in humans are considered to be mild or subclinical. However, during the recent epidemics in the Pacific Islands and the Americas, the infection was associated with Quillain-Barré syndrome and congenital infections with fetal ... ...

Abstract	Zika virus (ZIKV) infections in humans are considered to be mild or subclinical. However, during the recent epidemics in the Pacific Islands and the Americas, the infection was associated with Quillain-Barré syndrome and congenital infections with fetal brain abnormalities, including microcephaly. Thus, more detailed understanding of ZIKV-host cell interactions and regulation of innate immune responses by strains of differential evolutionary origin is required. Here, we characterized the infection and immune responses triggered by two epidemic Asian/American lineage viruses, including an isolate from fetal brains, and a historical, low passage 1947 African lineage virus in human monocyte-derived dendritic cells (DCs) and macrophages. The epidemic Asian/American ZIKV replicated well and induced relatively good antiviral responses in human DCs whereas the African strain replicated less efficiently and induced weaker immune responses. In macrophages both the African and Asian strains showed limited replication and relatively weak cytokine gene expression. Interestingly, in macrophages we observed host protein degradation, especially IRF3 and STAT2, at early phases of infection with both lineage viruses, suggesting an early proteasomal activation in phagocytic cells. Our data indicates that ZIKV evolution has led to significant phenotypic differences in the replication characteristics leading to differential regulation of host innate immune responses.
MeSH term(s)	Africa ; Asia ; Dendritic Cells/immunology ; Dendritic Cells/virology ; Evolution, Molecular ; Humans ; Immunity, Innate ; Macrophages/immunology ; Macrophages/virology ; Species Specificity ; Virus Replication ; Zika Virus/classification ; Zika Virus/immunology ; Zika Virus/physiology
Language	English
Publishing date	2019-10-31
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-52307-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Efficient replication and strong induction of innate immune responses by H9N2 avian influenza virus in human dendritic cells.

Westenius, Veera / Mäkelä, Sanna M / Ziegler, Thedi / Julkunen, Ilkka / Österlund, Pamela

Virology

2014 Volume 471-473, Page(s) 38–48

Abstract: Avian influenza A (H9N2) viruses have occasionally been identified in humans with upper respiratory tract infections. The novel H7N9/2013 virus identified in China shows that a low pathogenic avian influenza (LPAI) virus can be highly pathogenic in ... ...

Abstract	Avian influenza A (H9N2) viruses have occasionally been identified in humans with upper respiratory tract infections. The novel H7N9/2013 virus identified in China shows that a low pathogenic avian influenza (LPAI) virus can be highly pathogenic in humans. Therefore, it is important to understand virus-host cell interactions and immune responses triggered by LPAI viruses in humans. We found that LPAI A/Hong Kong/1073/99 (H9N2) virus replicated efficiently in human dendritic cells (DCs). The H9N2 virus induced strong IFN gene expression although with different kinetics than seasonal influenza A/Beijing/353/89 (H3N2) virus. IFN inducible antiviral proteins were produced in H9N2 virus-infected cells at the same level as in H3N2 infection. The H9N2 virus was extremely sensitive to the antiviral actions of type I IFNs. These results indicate that the avian influenza H9N2 virus is inducing a strong antiviral IFN response in human DCs.
MeSH term(s)	Blotting, Western ; Cells, Cultured ; Dendritic Cells/virology ; Enzyme-Linked Immunosorbent Assay ; Gene Expression Regulation, Viral/immunology ; Humans ; Immunity, Innate ; Influenza A Virus, H9N2 Subtype/physiology ; Interferons/genetics ; Interferons/metabolism ; Virus Cultivation ; Virus Replication/physiology
Chemical Substances	Interferons (9008-11-1)
Language	English
Publishing date	2014-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	200425-2
ISSN	1096-0341 ; 0042-6822
ISSN (online)	1096-0341
ISSN	0042-6822
DOI	10.1016/j.virol.2014.10.002
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ud II Zs.172: 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 ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Asian and African lineage Zika viruses show differential replication and innate immune responses in human dendritic cells and macrophages

Pamela Österlund / Miao Jiang / Veera Westenius / Suvi Kuivanen / Riia Järvi / Laura Kakkola / Rickard Lundberg / Krister Melén / Miša Korva / Tatjana Avšič – Županc / Olli Vapalahti / Ilkka Julkunen

Scientific Reports, Vol 9, Iss 1, Pp 1-

2019 Volume 15

Abstract: Abstract Zika virus (ZIKV) infections in humans are considered to be mild or subclinical. However, during the recent epidemics in the Pacific Islands and the Americas, the infection was associated with Quillain-Barré syndrome and congenital infections ... ...

Abstract	Abstract Zika virus (ZIKV) infections in humans are considered to be mild or subclinical. However, during the recent epidemics in the Pacific Islands and the Americas, the infection was associated with Quillain-Barré syndrome and congenital infections with fetal brain abnormalities, including microcephaly. Thus, more detailed understanding of ZIKV-host cell interactions and regulation of innate immune responses by strains of differential evolutionary origin is required. Here, we characterized the infection and immune responses triggered by two epidemic Asian/American lineage viruses, including an isolate from fetal brains, and a historical, low passage 1947 African lineage virus in human monocyte-derived dendritic cells (DCs) and macrophages. The epidemic Asian/American ZIKV replicated well and induced relatively good antiviral responses in human DCs whereas the African strain replicated less efficiently and induced weaker immune responses. In macrophages both the African and Asian strains showed limited replication and relatively weak cytokine gene expression. Interestingly, in macrophages we observed host protein degradation, especially IRF3 and STAT2, at early phases of infection with both lineage viruses, suggesting an early proteasomal activation in phagocytic cells. Our data indicates that ZIKV evolution has led to significant phenotypic differences in the replication characteristics leading to differential regulation of host innate immune responses.
Keywords	Medicine ; R ; Science ; Q
Subject code	570
Language	English
Publishing date	2019-10-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Middle East respiratory syndrome coronavirus shows poor replication but significant induction of antiviral responses in human monocyte-derived macrophages and dendritic cells.

Tynell, Janne / Westenius, Veera / Rönkkö, Esa / Munster, Vincent J / Melén, Krister / Österlund, Pamela / Julkunen, Ilkka

The Journal of general virology

2015 Volume 97, Issue 2, Page(s) 344–355

Abstract: In this study we assessed the ability of Middle East respiratory syndrome coronavirus (MERS-CoV) to replicate and induce innate immunity in human monocyte-derived macrophages and dendritic cells (MDDCs), and compared it with severe acute respiratory ... ...

Abstract	In this study we assessed the ability of Middle East respiratory syndrome coronavirus (MERS-CoV) to replicate and induce innate immunity in human monocyte-derived macrophages and dendritic cells (MDDCs), and compared it with severe acute respiratory syndrome coronavirus (SARS-CoV). Assessments of viral protein and RNA levels in infected cells showed that both viruses were impaired in their ability to replicate in these cells. Some induction of IFN-λ1, CXCL10 and MxA mRNAs in both macrophages and MDDCs was seen in response to MERS-CoV infection, but almost no such induction was observed in response to SARS-CoV infection. ELISA and Western blot assays showed clear production of CXCL10 and MxA in MERS-CoV-infected macrophages and MDDCs. Our data suggest that SARS-CoV and MERS-CoV replicate poorly in human macrophages and MDDCs, but MERS-CoV is nonetheless capable of inducing a readily detectable host innate immune response. Our results highlight a clear difference between the viruses in activating host innate immune responses in macrophages and MDDCs, which may contribute to the pathogenesis of infection.
MeSH term(s)	Adult ; Chemokine CXCL10/metabolism ; Dendritic Cells/immunology ; Dendritic Cells/virology ; Humans ; Immunity, Innate ; Macrophages/immunology ; Macrophages/virology ; Middle East Respiratory Syndrome Coronavirus/immunology ; Middle East Respiratory Syndrome Coronavirus/physiology ; Myxovirus Resistance Proteins/metabolism ; RNA, Viral/analysis ; SARS Virus/immunology ; SARS Virus/physiology ; Viral Proteins/analysis ; Virus Replication
Chemical Substances	CXCL10 protein, human ; Chemokine CXCL10 ; MX1 protein, human ; Myxovirus Resistance Proteins ; RNA, Viral ; Viral Proteins
Keywords	covid19
Language	English
Publishing date	2015-11-24
Publishing country	England
Document type	Comparative Study ; 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.0.000351
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 610: 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: RIG-I Signaling Is Essential for Influenza B Virus-Induced Rapid Interferon Gene Expression.

Mäkelä, Sanna M / Österlund, Pamela / Westenius, Veera / Latvala, Sinikka / Diamond, Michael S / Gale, Michael / Julkunen, Ilkka

Journal of virology

2015 Volume 89, Issue 23, Page(s) 12014–12025

Abstract: Unlabelled: Influenza B virus causes annual epidemics and, along with influenza A virus, accounts for substantial disease and economic burden throughout the world. Influenza B virus infects only humans and some marine mammals and is not responsible for ... ...

Abstract	Unlabelled: Influenza B virus causes annual epidemics and, along with influenza A virus, accounts for substantial disease and economic burden throughout the world. Influenza B virus infects only humans and some marine mammals and is not responsible for pandemics, possibly due to a very low frequency of reassortment and a lower evolutionary rate than that of influenza A virus. Influenza B virus has been less studied than influenza A virus, and thus, a comparison of influenza A and B virus infection mechanisms may provide new insight into virus-host interactions. Here we analyzed the early events in influenza B virus infection and interferon (IFN) gene expression in human monocyte-derived macrophages and dendritic cells. We show that influenza B virus induces IFN regulatory factor 3 (IRF3) activation and IFN-λ1 gene expression with faster kinetics than does influenza A virus, without a requirement for viral protein synthesis or replication. Influenza B virus-induced activation of IRF3 required the fusion of viral and endosomal membranes, and nuclear accumulation of IRF3 and viral NP occurred concurrently. In comparison, immediate early IRF3 activation was not observed in influenza A virus-infected macrophages. Experiments with RIG-I-, MDA5-, and RIG-I/MDA5-deficient mouse fibroblasts showed that RIG-I is the critical pattern recognition receptor needed for the influenza B virus-induced activation of IRF3. Our results show that innate immune mechanisms are activated immediately after influenza B virus entry through the endocytic pathway, whereas influenza A virus avoids early IRF3 activation and IFN gene induction. Importance: Recently, a great deal of interest has been paid to identifying the ligands for RIG-I under conditions of natural infection, as many previous studies have been based on transfection of cells with different types of viral or synthetic RNA structures. We shed light on this question by analyzing the earliest step in innate immune recognition of influenza B virus by human macrophages. We show that influenza B virus induces IRF3 activation, leading to IFN gene expression after viral RNPs (vRNPs) are released into the cytosol and are recognized by RIG-I receptor, meaning that the incoming influenza B virus is already able to activate IFN gene expression. In contrast, influenza A (H3N2) virus failed to activate IRF3 at very early times of infection, suggesting that there are differences in innate immune recognition between influenza A and B viruses.
MeSH term(s)	Animals ; Cell Line ; DEAD Box Protein 58 ; DEAD-box RNA Helicases/metabolism ; Dendritic Cells/immunology ; Gene Expression Regulation/immunology ; Host-Pathogen Interactions ; Humans ; Immunoblotting ; Influenza B virus/immunology ; Influenza, Human/immunology ; Interferon Regulatory Factor-3/genetics ; Interferon Regulatory Factor-3/metabolism ; Interferons ; Interleukins/immunology ; Interleukins/metabolism ; Macrophages/immunology ; Mice ; Mice, Knockout ; Microscopy, Fluorescence ; Real-Time Polymerase Chain Reaction ; Receptors, Immunologic ; Signal Transduction/immunology
Chemical Substances	interferon-lambda, human ; IRF3 protein, human ; Interferon Regulatory Factor-3 ; Interleukins ; Receptors, Immunologic ; Interferons (9008-11-1) ; RIGI protein, human (EC 3.6.1.-) ; DEAD Box Protein 58 (EC 3.6.4.13) ; DEAD-box RNA Helicases (EC 3.6.4.13)
Language	English
Publishing date	2015-09-16
Publishing country	United States
Document type	Journal Article ; 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.01576-15
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 609: 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

To top

More links

Kategorien

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

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito