Pöhlmann, Stefan

[["dc.bibliographiccitation.artnumber","e97695"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","PLOS ONE"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Eckert, Nadine"],["dc.contributor.author","Wrensch, Florian"],["dc.contributor.author","Gärtner, Sabine"],["dc.contributor.author","Palanisamy, Navaneethan"],["dc.contributor.author","Goedecke, Ulrike"],["dc.contributor.author","Jäger, Nils"],["dc.contributor.author","Pöhlmann, Stefan"],["dc.contributor.author","Winkler, Michael"],["dc.date.accessioned","2019-07-09T11:39:43Z"],["dc.date.available","2019-07-09T11:39:43Z"],["dc.date.issued","2014"],["dc.description.abstract","Reporter genes inserted into viral genomes enable the easy and rapid quantification of virus replication, which is instrumental to efficient in vitro screening of antiviral compounds or in vivo analysis of viral spread and pathogenesis. Based on a published design, we have generated several replication competent influenza A viruses carrying either fluorescent proteins or Gaussia luciferase. Reporter activity could be readily quantified in infected cultures, but the virus encoding Gaussia luciferase was more stable than viruses bearing fluorescent proteins and was therefore analyzed in detail. Quantification of Gaussia luciferase activity in the supernatants of infected culture allowed the convenient and highly sensitive detection of viral spread, and enzymatic activity correlated with the number of infectious particles released from infected cells. Furthermore, the Gaussia luciferase encoding virus allowed the sensitive quantification of the antiviral activity of the neuraminidase inhibitor (NAI) zanamivir and the host cell interferon-inducible transmembrane (IFITM) proteins 1–3, which are known to inhibit influenza virus entry. Finally, the virus was used to demonstrate that influenza A virus infection is sensitive to a modulator of endosomal cholesterol, in keeping with the concept that IFITMs inhibit viral entry by altering cholesterol levels in the endosomal membrane. In sum, we report the characterization of a novel influenza A reporter virus, which allows fast and sensitive detection of viral spread and its inhibition, and we show that influenza A virus entry is sensitive to alterations of endosomal cholesterol levels."],["dc.identifier.doi","10.1371/journal.pone.0097695"],["dc.identifier.pmid","24842154"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10118"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58030"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Influenza A Virus Encoding Secreted Gaussia Luciferase as Useful Tool to Analyze Viral Replication and Its Inhibition by Antiviral Compounds and Cellular Proteins"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0284"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Critical Care Explorations"],["dc.bibliographiccitation.lastpage","5"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Hofmann-Winkler, Heike"],["dc.contributor.author","Moerer, Onnen"],["dc.contributor.author","Alt-Epping, Sabine"],["dc.contributor.author","Bräuer, Anselm"],["dc.contributor.author","Büttner, Benedikt"],["dc.contributor.author","Müller, Martin"],["dc.contributor.author","Fricke, Torben"],["dc.contributor.author","Grundmann, Julian"],["dc.contributor.author","Harnisch, Lars-Olav"],["dc.contributor.author","Heise, Daniel"],["dc.contributor.author","Kernchen, Andrea"],["dc.contributor.author","Pressler, Meike"],["dc.contributor.author","Stephani, Caspar"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Kaul, Artur"],["dc.contributor.author","Gärtner, Sabine"],["dc.contributor.author","Kramer, Stefanie"],["dc.contributor.author","Pöhlmann, Stefan"],["dc.contributor.author","Winkler, Martin Sebastian"],["dc.date.accessioned","2020-11-27T11:23:20Z"],["dc.date.accessioned","2021-10-27T13:22:21Z"],["dc.date.available","2020-11-27T11:23:20Z"],["dc.date.available","2021-10-27T13:22:21Z"],["dc.date.issued","2020"],["dc.description.abstract","Objectives: Severe acute respiratory syndrome coronavirus 2 cell entry depends on angiotensin-converting enzyme 2 and transmembrane serine protease 2 and is blocked in cell culture by camostat mesylate, a clinically proven protease inhibitor. Whether camostat mesylate is able to lower disease burden in coronavirus disease 2019 sepsis is currently unknown. Design: Retrospective observational case series. Setting: Patient treated in ICU of University hospital Göttingen, Germany. Patients: Eleven critical ill coronavirus disease 2019 patients with organ failure were treated in ICU. Interventions: Compassionate use of camostat mesylate (six patients, camostat group) or hydroxychloroquine (five patients, hydroxychloroquine group). Measurements and Main Results: Clinical courses were assessed by Sepsis-related Organ Failure Assessment score at days 1, 3, and 8. Further, viral load, oxygenation, and inflammatory markers were determined. Sepsis-related Organ Failure Assessment score was comparable between camostat and hydroxychloroquine groups upon ICU admission. During observation, the Sepsis-related Organ Failure Assessment score decreased in the camostat group but remained elevated in the hydroxychloroquine group. The decline in disease severity in camostat mesylate treated patients was paralleled by a decline in inflammatory markers and improvement of oxygenation. Conclusions: The severity of coronavirus disease 2019 decreased upon camostat mesylate treatment within a period of 8 days and a similar effect was not observed in patients receiving hydroxychloroquine. Camostat mesylate thus warrants further evaluation within randomized clinical trials."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2020"],["dc.identifier.doi","10.1097/CCE.0000000000000284"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17663"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92088"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","2639-8028"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Camostat Mesylate May Reduce Severity of Coronavirus Disease 2019 Sepsis: A First Observation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3859"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Winkler, Michael"],["dc.contributor.author","Wrensch, Florian"],["dc.contributor.author","Bosch, Pascale"],["dc.contributor.author","Knoth, Maike"],["dc.contributor.author","Schindler, Michael"],["dc.contributor.author","Gärtner, Sabine"],["dc.contributor.author","Pöhlmann, Stefan"],["dc.date.accessioned","2020-12-10T18:47:09Z"],["dc.date.available","2020-12-10T18:47:09Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.3390/ijms20163859"],["dc.identifier.eissn","1422-0067"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16799"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78659"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Analysis of IFITM-IFITM Interactions by a Flow Cytometry-Based FRET Assay"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Virology Journal"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Lambertz, Ruth Lydia Olga"],["dc.contributor.author","Gerhauser, Ingo"],["dc.contributor.author","Nehlmeier, Inga"],["dc.contributor.author","Gärtner, Sabine"],["dc.contributor.author","Winkler, Michael"],["dc.contributor.author","Leist, Sarah Rebecca"],["dc.contributor.author","Kollmus, Heike"],["dc.contributor.author","Pöhlmann, Stefan"],["dc.contributor.author","Schughart, Klaus"],["dc.date.accessioned","2020-12-10T18:39:01Z"],["dc.date.available","2020-12-10T18:39:01Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1186/s12985-020-01323-z"],["dc.identifier.eissn","1743-422X"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17233"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77513"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","H2 influenza A virus is not pathogenic in Tmprss2 knock-out mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0224082"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Winkler, Michael"],["dc.contributor.author","Gärtner, Sabine"],["dc.contributor.author","Markus, Lara"],["dc.contributor.author","Hoffmann, Markus"],["dc.contributor.author","Nehlmeier, Inga"],["dc.contributor.author","Krawczak, Michael"],["dc.contributor.author","Sauermann, Ulrike"],["dc.contributor.author","Pöhlmann, Stefan"],["dc.date.accessioned","2019-11-05T08:51:28Z"],["dc.date.accessioned","2021-10-27T13:13:08Z"],["dc.date.available","2019-11-05T08:51:28Z"],["dc.date.available","2021-10-27T13:13:08Z"],["dc.date.issued","2019"],["dc.description.abstract","The experimental infection of rhesus macaques (rh) with simian immunodeficiency virus (SIV) is an important model for human immunodeficiency virus (HIV) infection of humans. The interferon-induced transmembrane protein 3 (IFITM3) inhibits HIV and SIV infection at the stage of host cell entry. However, it is still unclear to what extent the antiviral activity of IFITM3 observed in cell culture translates into inhibition of HIV/SIV spread in the infected host. We have shown previously that although rhIFITM3 inhibits SIV entry into cultured cells, polymorphisms in the rhIFITM3 gene are not strongly associated with viral load or disease progression in SIV infected macaques. Here, we examined whether rhIFITM3(2), which is closely related to rhIFITM3 at the sequence level, exerts antiviral activity and whether polymorphisms in the rhIFITM3(2) gene impact the course of SIV infection. We show that expression of rhIFITM3(2) is interferon-inducible and inhibits SIV entry into cells, although with reduced efficiency as compared to rhIFITM3. We further report the identification of 19 polymorphisms in the rhIFITM3(2) gene. However, analysis of a well characterized cohort of SIV infected macaques revealed that none of the polymorphisms had a significant impact upon the course of SIV infection. These results and our previous work suggest that polymorphisms in the rhIFITM3 and rhIFITM3(2) genes do not strongly modulate the course of SIV infection in macaques."],["dc.identifier.doi","10.1371/journal.pone.0224082"],["dc.identifier.pmid","31682595"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16596"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/91754"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","1932-6203"],["dc.relation.issn","1932-6203"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","599"],["dc.title","Role of rhesus macaque IFITM3(2) in simian immunodeficiency virus infection of macaques"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e01488-16"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Virology"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Wrensch, Florian"],["dc.contributor.author","Hoffmann, Markus"],["dc.contributor.author","Gärtner, Sabine"],["dc.contributor.author","Nehlmeier, Inga"],["dc.contributor.author","Winkler, Michael"],["dc.contributor.author","Pöhlmann, Stefan"],["dc.contributor.editor","Ross, Susan R."],["dc.date.accessioned","2022-10-06T13:25:35Z"],["dc.date.available","2022-10-06T13:25:35Z"],["dc.date.issued","2017"],["dc.description.abstract","ABSTRACT\n Interferon-induced transmembrane proteins (IFITMs) can inhibit the cellular entry of several enveloped viruses, including simian immunodeficiency virus (SIV). The blockade of SIV by IFITMs is isolate specific, raising the question of which parameters impact sensitivity to IFITM. We show that the virion context in which SIV-Env is presented and the efficiency of virion incorporation determine Env susceptibility to inhibition by IFITMs. Thus, determinants other than the nature of the envelope protein can impact the IFITM sensitivity of viral entry.\n \n IMPORTANCE\n The host cell-encoded IFITM proteins can block viral entry and are an important component of the innate defenses against viral infection. However, the determinants controlling whether a virus is susceptible to blockade by IFITM proteins are incompletely understood. Our study shows that the amount of envelope proteins incorporated into virions as well as the nature of the virion particle itself can impact the sensitivity of viral entry to IFITMs. These results show for the first time that determinants other than the viral envelope protein can impact sensitivity to IFITM and have implications for the interpretation of previously published data on inhibition of viruses by IFITM proteins. Moreover, our findings might help to define the mechanism underlying the antiviral activity of IFITM proteins."],["dc.description.sponsorship"," Leibniz-Gemeinschaft https://doi.org/10.13039/501100001664"],["dc.identifier.doi","10.1128/JVI.01488-16"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/114874"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.eissn","1098-5514"],["dc.relation.issn","0022-538X"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Virion Background and Efficiency of Virion Incorporation Determine Susceptibility of Simian Immunodeficiency Virus Env-Driven Viral Entry to Inhibition by IFITM Proteins"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0212757"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","PlOS ONE"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Bdeir, Najat"],["dc.contributor.author","Arora, Prerna"],["dc.contributor.author","Gärtner, Sabine"],["dc.contributor.author","Hoffmann, Markus"],["dc.contributor.author","Reichl, Udo"],["dc.contributor.author","Pöhlmann, Stefan"],["dc.contributor.author","Winkler, Michael"],["dc.date.accessioned","2019-07-09T11:50:20Z"],["dc.date.available","2019-07-09T11:50:20Z"],["dc.date.issued","2019"],["dc.description.abstract","Influenza A virus (IAV) infection poses a serious health threat and novel antiviral strategies are needed. Defective interfering particles (DIPs) can be generated in IAV infected cells due to errors of the viral polymerase and may suppress spread of wild type (wt) virus. The antiviral activity of DIPs is exerted by a DI genomic RNA segment that usually contains a large deletion and suppresses amplification of wt segments, potentially by competing for cellular and viral resources. DI-244 is a naturally occurring prototypic segment 1-derived DI RNA in which most of the PB2 open reading frame has been deleted and which is currently developed for antiviral therapy. At present, coinfection with wt virus is required for production of DI-244 particles which raises concerns regarding biosafety and may complicate interpretation of research results. Here, we show that cocultures of 293T and MDCK cell lines stably expressing codon optimized PB2 allow production of DI-244 particles solely from plasmids and in the absence of helper virus. Moreover, we demonstrate that infectivity of these particles can be quantified using MDCK-PB2 cells. Finally, we report that the DI-244 particles produced in this novel system exert potent antiviral activity against H1N1 and H3N2 IAV but not against the unrelated vesicular stomatitis virus. This is the first report of DIP production in the absence of infectious IAV and may spur efforts to develop DIPs for antiviral therapy."],["dc.identifier.doi","10.1371/journal.pone.0212757"],["dc.identifier.pmid","30822349"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15912"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59749"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","599"],["dc.title","A system for production of defective interfering particles in the absence of infectious influenza A virus"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0172847"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","PLOS ONE"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Winkler, Michael"],["dc.contributor.author","Gärtner, Sabine"],["dc.contributor.author","Wrensch, Florian"],["dc.contributor.author","Krawczak, Michael"],["dc.contributor.author","Sauermann, Ulrike"],["dc.contributor.author","Pöhlmann, Stefan"],["dc.date.accessioned","2019-07-09T11:43:17Z"],["dc.date.available","2019-07-09T11:43:17Z"],["dc.date.issued","2017"],["dc.description.abstract","nterferon-induced transmembrane proteins (IFITMs) have been recognized as important antiviral effectors of the innate immune system, both in cell culture and in infected humans. In particular, polymorphisms of the human IFITM3 gene have been shown to affect disease severity and progression in influenza A virus (FLUAV) and human immunodeficiency virus (HIV) infection, respectively. Rhesus macaques (Macaca mulatta) are commonly used to model human infections and the experimental inoculation of these animals with simian immunodeficiency virus (SIV) is one of the best models for HIV/AIDS in humans. However, information on the role of IFITM3 in SIV infection of rhesus macaques is currently lacking. We show that rhesus macaque (rh) IFITM3 inhibits SIV and FLUAV entry in cell culture, although with moderately reduced efficiency as compared to its human counterpart. We further report the identification of 16 polymorphisms in the rhIFITM3 gene, three of which were exonic and synonymous while the remainder was located in non-coding regions. Employing previously characterized samples from two cohorts of SIV-infected rhesus macaques, we investigated the relationship between these rhIFITM3 polymorphisms and both AIDS-free survival time and virus load. In cohort 1, several intronic polymorphisms were significantly associated with virus load or survival. However, an association with both parameters was not observed and significance was lost in most cases when animals were stratified for the presence of MHC allele Mamu-A1 001. Moreover, no significant genotype-phenotype associations were detected in cohort 2. These results suggest that, although IFITM3 can inhibit SIV infection in cell culture, genetic variation in rhIFITM3 might have only a minor impact on the course of SIV infection in experimentally infected animals."],["dc.identifier.doi","10.1371/journal.pone.0172847"],["dc.identifier.pmid","28257482"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14379"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58850"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Rhesus macaque IFITM3 gene polymorphisms and SIV infection"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","20477"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Bdeir, Najat"],["dc.contributor.author","Arora, Prerna"],["dc.contributor.author","Gärtner, Sabine"],["dc.contributor.author","Pöhlmann, Stefan"],["dc.contributor.author","Winkler, Michael"],["dc.date.accessioned","2021-12-01T09:23:45Z"],["dc.date.available","2021-12-01T09:23:45Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract Influenza A virus (IAV) infection constitutes a significant health threat. Defective interfering particles (DIPs) can arise during IAV infection and inhibit spread of wild type (WT) IAV. DIPs harbor defective RNA segments, termed DI RNAs, that usually contain internal deletions and interfere with replication of WT viral RNA segments. Here, we asked whether DIPs harboring two instead of one DI RNA exert increased antiviral activity. For this, we focused on DI RNAs derived from segments 1 and 3, which encode the polymerase subunits PB2 and PA, respectively. We demonstrate the successful production of DIPs harboring deletions in segments 1 and/or 3, using cell lines that co-express PB2 and PA. Further, we demonstrate that DIPs harboring two instead of one DI RNA do not exhibit increased ability to inhibit replication of a WT RNA segment. Similarly, the presence of two DI RNAs did not augment the induction of the interferon-stimulated gene MxA and the inhibition of IAV infection. Collectively, our findings suggest that the presence of multiple DI RNAs derived from genomic segments encoding polymerase subunits might not result in increased antiviral activity."],["dc.description.abstract","Abstract Influenza A virus (IAV) infection constitutes a significant health threat. Defective interfering particles (DIPs) can arise during IAV infection and inhibit spread of wild type (WT) IAV. DIPs harbor defective RNA segments, termed DI RNAs, that usually contain internal deletions and interfere with replication of WT viral RNA segments. Here, we asked whether DIPs harboring two instead of one DI RNA exert increased antiviral activity. For this, we focused on DI RNAs derived from segments 1 and 3, which encode the polymerase subunits PB2 and PA, respectively. We demonstrate the successful production of DIPs harboring deletions in segments 1 and/or 3, using cell lines that co-express PB2 and PA. Further, we demonstrate that DIPs harboring two instead of one DI RNA do not exhibit increased ability to inhibit replication of a WT RNA segment. Similarly, the presence of two DI RNAs did not augment the induction of the interferon-stimulated gene MxA and the inhibition of IAV infection. Collectively, our findings suggest that the presence of multiple DI RNAs derived from genomic segments encoding polymerase subunits might not result in increased antiviral activity."],["dc.identifier.doi","10.1038/s41598-021-99691-1"],["dc.identifier.pii","99691"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94746"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","2045-2322"],["dc.title","Evidence that two instead of one defective interfering RNA in influenza A virus-derived defective interfering particles (DIPs) does not enhance antiviral activity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1026"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Viruses"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Chukhno, Ekaterina"],["dc.contributor.author","Gärtner, Sabine"],["dc.contributor.author","Rahman Siregar, Abdul"],["dc.contributor.author","Mehr, Alexander"],["dc.contributor.author","Wende, Marie"],["dc.contributor.author","Petkov, Stoyan"],["dc.contributor.author","Götting, Jasper"],["dc.contributor.author","Dhingra, Akshay"],["dc.contributor.author","Schulz, Thomas"],["dc.contributor.author","Pöhlmann, Stefan"],["dc.contributor.author","Winkler, Michael"],["dc.date.accessioned","2020-12-10T18:47:24Z"],["dc.date.available","2020-12-10T18:47:24Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.3390/v11111026"],["dc.identifier.eissn","1999-4915"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17113"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78754"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","A Fosmid-Based System for the Generation of Recombinant Cercopithecine Alphaherpesvirus 2 Encoding Reporter Genes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]