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Article ; Online: Direct translation of incoming retroviral genomes.

Köppke, Julia / Keller, Luise-Elektra / Stuck, Michelle / Arnow, Nicolas D / Bannert, Norbert / Doellinger, Joerg / Cingöz, Oya

Nature communications

2024 Volume 15, Issue 1, Page(s) 299

Abstract: Viruses that carry a positive-sense, single-stranded (+ssRNA) RNA translate their genomes soon after entering the host cell to produce viral proteins, with the exception of retroviruses. A distinguishing feature of retroviruses is reverse transcription, ... ...

Abstract	Viruses that carry a positive-sense, single-stranded (+ssRNA) RNA translate their genomes soon after entering the host cell to produce viral proteins, with the exception of retroviruses. A distinguishing feature of retroviruses is reverse transcription, where the +ssRNA genome serves as a template to synthesize a double-stranded DNA copy that subsequently integrates into the host genome. As retroviral RNAs are produced by the host cell transcriptional machinery and are largely indistinguishable from cellular mRNAs, we investigated the potential of incoming retroviral genomes to directly express proteins. Here we show through multiple, complementary methods that retroviral genomes are translated after entry. Our findings challenge the notion that retroviruses require reverse transcription to produce viral proteins. Synthesis of retroviral proteins in the absence of productive infection has significant implications for basic retrovirology, immune responses and gene therapy applications.
MeSH term(s)	Retroviridae/genetics ; RNA ; Genetic Therapy ; RNA, Messenger/genetics ; Viral Proteins
Chemical Substances	RNA (63231-63-0) ; RNA, Messenger ; Viral Proteins
Language	English
Publishing date	2024-01-05
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-44501-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: HIV-1 Is a Poor Inducer of Innate Immune Responses.

Cingöz, Oya / Goff, Stephen P

mBio

2019 Volume 10, Issue 1

Abstract: Effective host immune responses against viral infection rely on the detection of the virus, activation of downstream signaling pathways, and the secretion of interferons (IFNs) and other cytokines. Many viruses can potently stimulate these responses, ... ...

Abstract	Effective host immune responses against viral infection rely on the detection of the virus, activation of downstream signaling pathways, and the secretion of interferons (IFNs) and other cytokines. Many viruses can potently stimulate these responses, whereas the immune response against human immunodeficiency virus type 1 (HIV-1) remains relatively less well characterized. Here we show that HIV-1 infection with reporter viruses does not activate sensing pathways in cell lines and primary cells that are otherwise responsive to foreign nucleic acids. After entry into cells, reverse transcription and reporter expression occur without the virus ever being detected by cellular sensors or stimulating an interferon response. Using multiple methods, including the use of reporter cell lines for type I IFN and NF-κB pathway activation, quantifying mRNA levels for IFN-stimulated genes (ISGs), and assaying for markers of innate immune activation, we show that single-round pseudotyped HIV-1-based reporter viruses fail to induce innate immune responses.
MeSH term(s)	Biomarkers/analysis ; Cells, Cultured ; Gene Expression Profiling ; HIV Infections/immunology ; HIV-1/immunology ; Humans ; Immunity, Innate ; Models, Biological
Chemical Substances	Biomarkers
Language	English
Publishing date	2019-02-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mBio.02834-18
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Article ; Online: Direct translation of incoming retroviral genomes

Julia Köppke / Luise-Elektra Keller / Michelle Stuck / Nicolas D. Arnow / Norbert Bannert / Joerg Doellinger / Oya Cingöz

Nature Communications, Vol 15, Iss 1, Pp 1-

2024 Volume 12

Abstract: Abstract Viruses that carry a positive-sense, single-stranded (+ssRNA) RNA translate their genomes soon after entering the host cell to produce viral proteins, with the exception of retroviruses. A distinguishing feature of retroviruses is reverse ... ...

Abstract	Abstract Viruses that carry a positive-sense, single-stranded (+ssRNA) RNA translate their genomes soon after entering the host cell to produce viral proteins, with the exception of retroviruses. A distinguishing feature of retroviruses is reverse transcription, where the +ssRNA genome serves as a template to synthesize a double-stranded DNA copy that subsequently integrates into the host genome. As retroviral RNAs are produced by the host cell transcriptional machinery and are largely indistinguishable from cellular mRNAs, we investigated the potential of incoming retroviral genomes to directly express proteins. Here we show through multiple, complementary methods that retroviral genomes are translated after entry. Our findings challenge the notion that retroviruses require reverse transcription to produce viral proteins. Synthesis of retroviral proteins in the absence of productive infection has significant implications for basic retrovirology, immune responses and gene therapy applications.
Keywords	Science ; Q
Subject code	570
Language	English
Publishing date	2024-01-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Cyclin-dependent kinase activity is required for type I interferon production.

Cingöz, Oya / Goff, Stephen P

Proceedings of the National Academy of Sciences of the United States of America

2018 Volume 115, Issue 13, Page(s) E2950–E2959

Abstract: Recognition of nucleic acids results in the production of type I IFNs, which activate the JAK/STAT pathway and promote the expression of IFN-stimulated genes. In a search for modulators of this pathway, we discovered an unexpected requirement for cyclin- ... ...

Abstract	Recognition of nucleic acids results in the production of type I IFNs, which activate the JAK/STAT pathway and promote the expression of IFN-stimulated genes. In a search for modulators of this pathway, we discovered an unexpected requirement for cyclin-dependent kinases (CDK) in the production of type I IFN following nucleic acid sensing and virus infection. Inhibition of CDK activity or knockdown of CDK levels leads to a striking block in STAT activation and IFN-stimulated gene expression. CDKs are not required for the initial nucleic acid sensing leading to IFN-β mRNA induction, nor for the response to exogenous IFN-α/β, but are critical for IFN-β release into culture supernatants, suggesting a posttranscriptional role for CDKs in type I IFN production. In the absence of CDK activity, we demonstrate a translational block specific for IFN-β, in which IFN-β mRNA is removed from the actively translating polysomes, while the distribution of other cellular mRNAs or global translation rates are unaffected. Our findings reveal a critical role for CDKs in the translation of IFN-β.
MeSH term(s)	Antiviral Agents/pharmacology ; Cells, Cultured ; Cyclin-Dependent Kinases/genetics ; Cyclin-Dependent Kinases/metabolism ; Humans ; Immunity, Innate/drug effects ; Immunity, Innate/immunology ; Interferon-alpha/pharmacology ; Interferon-beta/pharmacology ; Phosphorylation/drug effects ; STAT1 Transcription Factor/genetics ; STAT1 Transcription Factor/metabolism ; Signal Transduction/drug effects
Chemical Substances	Antiviral Agents ; Interferon-alpha ; STAT1 Transcription Factor ; Interferon-beta (77238-31-4) ; Cyclin-Dependent Kinases (EC 2.7.11.22)
Language	English
Publishing date	2018-03-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1720431115
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Article ; Online: Vpx enhances innate immune responses independently of SAMHD1 during HIV-1 infection.

Cingöz, Oya / Arnow, Nicolas D / Puig Torrents, Mireia / Bannert, Norbert

Retrovirology

2021 Volume 18, Issue 1, Page(s) 4

Abstract: Background: The genomes of HIV-2 and some SIV strains contain the accessory gene vpx, which carries out several functions during infection, including the downregulation of SAMHD1. Vpx is also commonly used in experiments to increase HIV-1 infection ... ...

Abstract	Background: The genomes of HIV-2 and some SIV strains contain the accessory gene vpx, which carries out several functions during infection, including the downregulation of SAMHD1. Vpx is also commonly used in experiments to increase HIV-1 infection efficiency in myeloid cells, particularly in studies that investigate the activation of antiviral pathways. However, the potential effects of Vpx on cellular innate immune signaling is not completely understood. We investigated whether and how Vpx affects ISG responses in monocytic cell lines and MDMs during HIV-1 infection. Results: HIV-1 infection at excessively high virus doses can induce ISG activation, although at the expense of high levels of cell death. At equal infection levels, the ISG response is potentiated by the presence of Vpx and requires the initiation of reverse transcription. The interaction of Vpx with the DCAF1 adaptor protein is important for the enhanced response, implicating Vpx-mediated degradation of a host factor. Cells lacking SAMHD1 show similarly augmented responses, suggesting an effect that is independent of SAMHD1 degradation. Overcoming SAMHD1 restriction in MDMs to reach equal infection levels with viruses containing and lacking Vpx reveals a novel function of Vpx in elevating innate immune responses. Conclusions: Vpx likely has as yet undefined roles in infected cells. Our results demonstrate that Vpx enhances ISG responses in myeloid cell lines and primary cells independently of its ability to degrade SAMHD1. These findings have implications for innate immunity studies in myeloid cells that use Vpx delivery with HIV-1 infection.
MeSH term(s)	Cell Line ; HEK293 Cells ; HIV Infections/genetics ; HIV Infections/immunology ; HIV-2/genetics ; HIV-2/physiology ; Host-Pathogen Interactions/genetics ; Host-Pathogen Interactions/immunology ; Humans ; Immunity, Innate/genetics ; Leukocytes, Mononuclear/virology ; Proteolysis ; SAM Domain and HD Domain-Containing Protein 1/genetics ; SAM Domain and HD Domain-Containing Protein 1/immunology ; SAM Domain and HD Domain-Containing Protein 1/metabolism ; THP-1 Cells ; Viral Regulatory and Accessory Proteins/genetics ; Viral Regulatory and Accessory Proteins/immunology ; Virus Replication
Chemical Substances	VPX protein, Human immunodeficiency virus 2 ; Viral Regulatory and Accessory Proteins ; SAM Domain and HD Domain-Containing Protein 1 (EC 3.1.5.-) ; SAMHD1 protein, human (EC 3.1.5.-)
Language	English
Publishing date	2021-02-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1742-4690
ISSN (online)	1742-4690
DOI	10.1186/s12977-021-00548-2
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Vpx enhances innate immune responses independently of SAMHD1 during HIV-1 infection

Cingöz, Oya / Arnow, Nicolas D. / Torrents, Mireia Puig / Bannert, Norbert

2021

Abstract: Background The genomes of HIV-2 and some SIV strains contain the accessory gene vpx, which carries out several functions during infection, including the downregulation of SAMHD1. Vpx is also commonly used in experiments to increase HIV-1 infection ... ...

Abstract	Background The genomes of HIV-2 and some SIV strains contain the accessory gene vpx, which carries out several functions during infection, including the downregulation of SAMHD1. Vpx is also commonly used in experiments to increase HIV-1 infection efficiency in myeloid cells, particularly in studies that investigate the activation of antiviral pathways. However, the potential effects of Vpx on cellular innate immune signaling is not completely understood. We investigated whether and how Vpx affects ISG responses in monocytic cell lines and MDMs during HIV-1 infection. Results HIV-1 infection at excessively high virus doses can induce ISG activation, although at the expense of high levels of cell death. At equal infection levels, the ISG response is potentiated by the presence of Vpx and requires the initiation of reverse transcription. The interaction of Vpx with the DCAF1 adaptor protein is important for the enhanced response, implicating Vpx-mediated degradation of a host factor. Cells lacking SAMHD1 show similarly augmented responses, suggesting an effect that is independent of SAMHD1 degradation. Overcoming SAMHD1 restriction in MDMs to reach equal infection levels with viruses containing and lacking Vpx reveals a novel function of Vpx in elevating innate immune responses. Conclusions Vpx likely has as yet undefined roles in infected cells. Our results demonstrate that Vpx enhances ISG responses in myeloid cell lines and primary cells independently of its ability to degrade SAMHD1. These findings have implications for innate immunity studies in myeloid cells that use Vpx delivery with HIV-1 infection. Peer Reviewed
Keywords	Infection ; Innate immunity ; Interferon ; MDM ; Macrophage ; THP-1 ; ISG ; ISRE ; 610 Medizin und Gesundheit ; ddc:610
Subject code	570
Language	English
Publishing date	2021-02-09
Publisher	Robert Koch-Institut
Publishing country	de
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Ustekinumab.

Cingoz, Oya

mAbs

2010 Volume 1, Issue 3, Page(s) 216–221

Abstract: Ustekinumab is an anti-IL12/23 IgG1 kappa human monoclonal antibody currently undergoing US Food and Drug Administration review for use as a psoriasis treatment. The candidate has also been evaluated in Phase 2 studies as a treatment for psoriatic ... ...

Abstract	Ustekinumab is an anti-IL12/23 IgG1 kappa human monoclonal antibody currently undergoing US Food and Drug Administration review for use as a psoriasis treatment. The candidate has also been evaluated in Phase 2 studies as a treatment for psoriatic arthritis, Crohn disease and multiple sclerosis.In large clinical trials, ustekinumab has proven effective for treating moderate to severe plaque psoriasis. Although long-term follow-up studies are needed to address safety concerns, the hopes are high for psoriasis treatment. Ustekinumab has recently been approved for marketing in Canada and Europe.
MeSH term(s)	Animals ; Antibodies, Monoclonal/adverse effects ; Antibodies, Monoclonal/therapeutic use ; Antibodies, Monoclonal, Humanized ; Arthritis, Psoriatic/drug therapy ; Arthritis, Psoriatic/immunology ; Canada ; Clinical Trials as Topic ; Crohn Disease/drug therapy ; Crohn Disease/immunology ; Drug Approval ; Europe ; Humans ; I-kappa B Proteins/immunology ; NF-KappaB Inhibitor alpha ; NF-kappa B/antagonists & inhibitors ; United States ; Ustekinumab
Chemical Substances	Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; I-kappa B Proteins ; NF-kappa B ; NFKBIA protein, human ; NF-KappaB Inhibitor alpha (139874-52-5) ; Ustekinumab (FU77B4U5Z0)
Language	English
Publishing date	2010-01-12
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2537838-7
ISSN	1942-0870 ; 1942-0870
ISSN (online)	1942-0870
ISSN	1942-0870
DOI	10.4161/mabs.1.3.8593
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: NP220 mediates silencing of unintegrated retroviral DNA.

Zhu, Yiping / Wang, Gary Z / Cingöz, Oya / Goff, Stephen P

Nature

2018 Volume 564, Issue 7735, Page(s) 278–282

Abstract: The entry of foreign DNA into many mammalian cell types triggers the innate immune system, a complex set of responses to prevent infection by pathogens. One aspect of the response is the potent epigenetic silencing of incoming viral ... ...

Abstract	The entry of foreign DNA into many mammalian cell types triggers the innate immune system, a complex set of responses to prevent infection by pathogens. One aspect of the response is the potent epigenetic silencing of incoming viral DNAs
MeSH term(s)	Antigens, Neoplasm/metabolism ; CRISPR-Associated Protein 9/genetics ; CRISPR-Associated Protein 9/metabolism ; Chromatin Immunoprecipitation ; Clustered Regularly Interspaced Short Palindromic Repeats/genetics ; DNA, Viral/genetics ; DNA-Binding Proteins/metabolism ; Gene Silencing ; Histone Deacetylase 1/metabolism ; Histone Deacetylases/metabolism ; Histone-Lysine N-Methyltransferase ; Humans ; Multiprotein Complexes/metabolism ; Nuclear Proteins/metabolism ; Phosphoproteins/metabolism ; Protein Methyltransferases/metabolism ; Proviruses/genetics ; RNA-Binding Proteins ; Repressor Proteins/metabolism ; Retroviridae/genetics ; Transcription Factors ; Virus Integration
Chemical Substances	Antigens, Neoplasm ; DNA, Viral ; DNA-Binding Proteins ; MPHOSPH8 protein, human ; Multiprotein Complexes ; Nuclear Proteins ; PPHLN1 protein, human ; Phosphoproteins ; RNA-Binding Proteins ; Repressor Proteins ; TASOR protein, human ; Transcription Factors ; ZNF638 protein, human ; Protein Methyltransferases (EC 2.1.1.-) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43) ; SETDB1 protein, human (EC 2.1.1.43) ; CRISPR-Associated Protein 9 (EC 3.1.-) ; HDAC1 protein, human (EC 3.5.1.98) ; HDAC4 protein, human (EC 3.5.1.98) ; Histone Deacetylase 1 (EC 3.5.1.98) ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2018-11-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-018-0750-6
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Zs.A 26: 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)
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Article ; Online: Characterization of interaction between Trim28 and YY1 in silencing proviral DNA of Moloney murine leukemia virus.

Lee, Andreia / CingÖz, Oya / Sabo, Yosef / Goff, Stephen P

Virology

2018 Volume 516, Page(s) 165–175

Abstract: Moloney Murine Leukemia Virus (M-MLV) proviral DNA is transcriptionally silenced in embryonic cells by a large repressor complex tethered to the provirus by two sequence-specific DNA binding proteins, ZFP809 and YY1. A central component of the complex is ...

Abstract	Moloney Murine Leukemia Virus (M-MLV) proviral DNA is transcriptionally silenced in embryonic cells by a large repressor complex tethered to the provirus by two sequence-specific DNA binding proteins, ZFP809 and YY1. A central component of the complex is Trim28, a scaffold protein that regulates many target genes involved in cell cycle progression, DNA damage responses, and viral gene expression. The silencing activity of Trim28, and its interactions with corepressors are often regulated by post-translational modifications such as sumoylation and phosphorylation. We defined the interaction domains of Trim28 and YY1, and investigated the role of sumoylation and phosphorylation of Trim28 in mediating M-MLV silencing. The RBCC domain of Trim28 was sufficient for interaction with YY1, and acidic region 1 and zinc fingers of YY1 were necessary and sufficient for its interaction with Trim28. Additionally, we found that residue K779 was critical for Trim28-mediated silencing of M-MLV in embryonic cells.
MeSH term(s)	Amino Acid Motifs ; Animals ; Gene Silencing ; Mice ; Moloney murine leukemia virus/genetics ; Moloney murine leukemia virus/physiology ; Protein Binding ; Protein Domains ; Proviruses/genetics ; Proviruses/metabolism ; Retroviridae Infections/genetics ; Retroviridae Infections/metabolism ; Retroviridae Infections/veterinary ; Retroviridae Infections/virology ; Rodent Diseases/genetics ; Rodent Diseases/metabolism ; Rodent Diseases/virology ; Tripartite Motif-Containing Protein 28/chemistry ; Tripartite Motif-Containing Protein 28/genetics ; Tripartite Motif-Containing Protein 28/metabolism ; YY1 Transcription Factor/chemistry ; YY1 Transcription Factor/genetics ; YY1 Transcription Factor/metabolism
Chemical Substances	YY1 Transcription Factor ; Yy1 protein, mouse ; Tripartite Motif-Containing Protein 28 (EC 2.3.2.27)
Language	English
Publishing date	2018-01-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; 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.2018.01.012
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Article ; Online: Motavizumab.

Cingoz, Oya

mAbs

2009 Volume 1, Issue 5, Page(s) 439–442

Abstract: Motavizumab (MEDI-524, Numax) is a second generation monoclonal antibody (mAb) derived from palivizumab (Synagis) using affinity maturation techniques. Motavizumab is currently undergoing US Food and Drug Administration review as a treatment for ... ...

Abstract	Motavizumab (MEDI-524, Numax) is a second generation monoclonal antibody (mAb) derived from palivizumab (Synagis) using affinity maturation techniques. Motavizumab is currently undergoing US Food and Drug Administration review as a treatment for respiratory syncytial virus (RSV) prophylaxis. It has been evaluated in large-scale clinical studies, and has demonstrated efficacy in reducing the disease burden of RSV in high-risk infant populations.
MeSH term(s)	Antibodies, Monoclonal/administration & dosage ; Antibodies, Monoclonal/adverse effects ; Antibodies, Monoclonal/immunology ; Antibodies, Monoclonal/therapeutic use ; Antibodies, Monoclonal, Humanized ; Child, Preschool ; Clinical Trials as Topic ; Humans ; Infant ; Infant, Newborn ; Respiratory Syncytial Virus Infections/drug therapy ; Respiratory Syncytial Virus Infections/immunology ; Respiratory Syncytial Virus Infections/prevention & control ; Respiratory Syncytial Virus, Human/immunology ; Treatment Outcome
Chemical Substances	Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; motavizumab (50Y163LK8Q)
Language	English
Publishing date	2009-09-10
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2537838-7
ISSN	1942-0870 ; 1942-0870
ISSN (online)	1942-0870
ISSN	1942-0870
DOI	10.4161/mabs.1.5.9496
Database	MEDical Literature Analysis and Retrieval System OnLINE

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