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  1. Article ; Online: Mechanisms of innate immune evasion in re-emerging RNA viruses.

    Ma, Daphne Y / Suthar, Mehul S

    Current opinion in virology

    2015  Volume 12, Page(s) 26–37

    Abstract: Recent outbreaks of Ebola, West Nile, Chikungunya, Middle Eastern Respiratory and other emerging/re-emerging RNA viruses continue to highlight the need to further understand the virus-host interactions that govern disease severity and infection outcome. ... ...

    Abstract Recent outbreaks of Ebola, West Nile, Chikungunya, Middle Eastern Respiratory and other emerging/re-emerging RNA viruses continue to highlight the need to further understand the virus-host interactions that govern disease severity and infection outcome. As part of the early host antiviral defense, the innate immune system mediates pathogen recognition and initiation of potent antiviral programs that serve to limit virus replication, limit virus spread and activate adaptive immune responses. Concordantly, viral pathogens have evolved several strategies to counteract pathogen recognition and cell-intrinsic antiviral responses. In this review, we highlight the major mechanisms of innate immune evasion by emerging and re-emerging RNA viruses, focusing on pathogens that pose significant risk to public health.
    MeSH term(s) Animals ; Communicable Diseases, Emerging/immunology ; Communicable Diseases, Emerging/virology ; Host-Pathogen Interactions ; Humans ; Immune Evasion ; Immunity, Innate ; Interferons/metabolism ; RNA Virus Infections/immunology ; RNA Virus Infections/metabolism ; RNA Virus Infections/virology ; RNA Viruses/immunology ; RNA Viruses/pathogenicity ; RNA Viruses/physiology ; Receptors, Pattern Recognition/metabolism ; Signal Transduction ; Virus Replication
    Chemical Substances Receptors, Pattern Recognition ; Interferons (9008-11-1)
    Keywords covid19
    Language English
    Publishing date 2015-06
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2611378-8
    ISSN 1879-6265 ; 1879-6257
    ISSN (online) 1879-6265
    ISSN 1879-6257
    DOI 10.1016/j.coviro.2015.02.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Conserved allosteric inhibitory site on the respiratory syncytial virus and human metapneumovirus RNA-dependent RNA polymerases.

    Kleiner, Victoria A / O Fischmann, Thierry / Howe, John A / Beshore, Douglas C / Eddins, Michael J / Hou, Yan / Mayhood, Todd / Klein, Daniel / Nahas, Debbie D / Lucas, Bob J / Xi, He / Murray, Edward / Ma, Daphne Y / Getty, Krista / Fearns, Rachel

    Communications biology

    2023  Volume 6, Issue 1, Page(s) 649

    Abstract: Respiratory syncytial virus (RSV) and human metapneumovirus (HMPV) are related RNA viruses responsible for severe respiratory infections and resulting disease in infants, elderly, and immunocompromised ... ...

    Abstract Respiratory syncytial virus (RSV) and human metapneumovirus (HMPV) are related RNA viruses responsible for severe respiratory infections and resulting disease in infants, elderly, and immunocompromised adults
    MeSH term(s) Infant ; Adult ; Humans ; Aged ; Metapneumovirus/genetics ; Metapneumovirus/metabolism ; RNA-Dependent RNA Polymerase/genetics ; RNA-Dependent RNA Polymerase/metabolism ; Respiratory Syncytial Virus, Human ; Respiratory Tract Infections ; RNA, Messenger
    Chemical Substances RNA-Dependent RNA Polymerase (EC 2.7.7.48) ; RNA, Messenger
    Language English
    Publishing date 2023-06-19
    Publishing country England
    Document type Journal Article
    ISSN 2399-3642
    ISSN (online) 2399-3642
    DOI 10.1038/s42003-023-04990-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: The molecular epidemiology of Treponema pallidum subspecies pallidum.

    Ma, Daphne Y / Giacani, Lorenzo / Centurión-Lara, Arturo

    Sexual health

    2015  Volume 12, Issue 2, Page(s) 141–147

    Abstract: Pathogens adapt and evolve in response to pressures exerted by host environments, leading to generation of genetically diverse variants. Treponema pallidum subspecies pallidum displays a substantial amount of interstrain diversity. These variants have ... ...

    Abstract Pathogens adapt and evolve in response to pressures exerted by host environments, leading to generation of genetically diverse variants. Treponema pallidum subspecies pallidum displays a substantial amount of interstrain diversity. These variants have been identified in various parts of the world, indicating transmission linkage between geographical regions. Genotyping is based on molecular characterisation of various loci in the syphilis treponeme genome, but still require further development and continued research, as new bacterial types are continually being detected. The goal for studying the molecular epidemiology of Treponema pallidum variants is the global monitoring of the transmission of genetically distinct organisms with different drug sensitivities and, potentially, different virulence proprieties.
    Language English
    Publishing date 2015-03-08
    Publishing country Australia
    Document type Journal Article
    ZDB-ID 2256731-8
    ISSN 1449-8987 ; 1448-5028
    ISSN (online) 1449-8987
    ISSN 1448-5028
    DOI 10.1071/SH14197
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6421: 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)

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  4. Article ; Online: The role of CD40 and CD154/CD40L in dendritic cells.

    Ma, Daphne Y / Clark, Edward A

    Seminars in immunology

    2009  Volume 21, Issue 5, Page(s) 265–272

    Abstract: In this review, we focus on the function of CD40-CD40L (CD154) interactions in the regulation of dendritic cell (DC)-T cell and DC-B cell crosstalk. In addition, we examine differences and similarities between the CD40 signaling pathway in DCs and other ... ...

    Abstract In this review, we focus on the function of CD40-CD40L (CD154) interactions in the regulation of dendritic cell (DC)-T cell and DC-B cell crosstalk. In addition, we examine differences and similarities between the CD40 signaling pathway in DCs and other innate immune cell receptors, and how these pathways integrate DC functions. As research into DC vaccines and immunotherapies progresses, further understanding of CD40 and DC function will advance the applicability of DCs in immunotherapy for human diseases.
    MeSH term(s) Animals ; B-Lymphocytes/immunology ; CD40 Antigens/immunology ; CD40 Ligand/immunology ; Cell Communication/immunology ; Dendritic Cells/immunology ; Humans ; Receptor Cross-Talk/immunology ; Signal Transduction/immunology ; T-Lymphocytes/immunology
    Chemical Substances CD40 Antigens ; CD40 Ligand (147205-72-9)
    Language English
    Publishing date 2009-06-12
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 1018141-6
    ISSN 1096-3618 ; 1044-5323
    ISSN (online) 1096-3618
    ISSN 1044-5323
    DOI 10.1016/j.smim.2009.05.010
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2843: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: CD22 is required for protection against West Nile virus Infection.

    Ma, Daphne Y / Suthar, Mehul S / Kasahara, Shinji / Gale, Michael / Clark, Edward A

    Journal of virology

    2013  Volume 87, Issue 6, Page(s) 3361–3375

    Abstract: West Nile virus (WNV) is a RNA virus of the family Flaviviridae and the leading cause of mosquito-borne encephalitis in the United States. Humoral immunity is essential for protection against WNV infection; however, the requirements for initiating ... ...

    Abstract West Nile virus (WNV) is a RNA virus of the family Flaviviridae and the leading cause of mosquito-borne encephalitis in the United States. Humoral immunity is essential for protection against WNV infection; however, the requirements for initiating effective antibody responses against WNV infection are still unclear. CD22 (Siglec-2) is expressed on B cells and regulates B cell receptor signaling, cell survival, proliferation, and antibody production. In this study, we investigated how CD22 contributes to protection against WNV infection and found that CD22 knockout (Cd22(-/-)) mice were highly susceptible to WNV infection and had increased viral loads in the serum and central nervous system (CNS) compared to wild-type (WT) mice. This was not due to a defect in humoral immunity, as Cd22(-/-) mice had normal WNV-specific antibody responses. However, Cd22(-/-) mice had decreased WNV-specific CD8(+) T cell responses compared to those of WT mice. These defects were not simply due to reduced cytotoxic activity or increased cell death but, rather, were associated with decreased lymphocyte migration into the draining lymph nodes (dLNs) of infected Cd22(-/-) mice. Cd22(-/-) mice had reduced production of the chemokine CCL3 in the dLNs after infection, suggesting that CD22 affects chemotaxis via controlling chemokine production. CD22 was not restricted to B cells but was also expressed on a subset of splenic DCIR2(+) dendritic cells that rapidly expand early after WNV infection. Thus, CD22 plays an essential role in controlling WNV infection by governing cell migration and CD8(+) T cell responses.
    MeSH term(s) Animals ; Antibodies, Viral/blood ; Blood/virology ; CD8-Positive T-Lymphocytes/immunology ; Central Nervous System/virology ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Sialic Acid Binding Ig-like Lectin 2/deficiency ; Sialic Acid Binding Ig-like Lectin 2/immunology ; Sialic Acid Binding Ig-like Lectin 2/metabolism ; Viral Load ; West Nile Fever/immunology ; West Nile virus/immunology
    Chemical Substances Antibodies, Viral ; Cd22 protein, mouse ; Sialic Acid Binding Ig-like Lectin 2
    Language English
    Publishing date 2013-01-09
    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.02368-12
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    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)

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  6. Article ; Online: Nitric oxide controls an inflammatory-like Ly6C(hi)PDCA1+ DC subset that regulates Th1 immune responses.

    Giordano, Daniela / Li, Chang / Suthar, Mehul S / Draves, Kevin E / Ma, Daphne Y / Gale, Michael / Clark, Edward A

    Journal of leukocyte biology

    2010  Volume 89, Issue 3, Page(s) 443–455

    Abstract: Using NOS2 KO mice, we investigated the hypothesis that NO modulation of BM-DC contributes to the NO-mediated control of Th1 immune responses. BM-DCs from NOS2 KO mice, compared with WT BM-DCs, have enhanced survival and responsiveness to TLR agonists, ... ...

    Abstract Using NOS2 KO mice, we investigated the hypothesis that NO modulation of BM-DC contributes to the NO-mediated control of Th1 immune responses. BM-DCs from NOS2 KO mice, compared with WT BM-DCs, have enhanced survival and responsiveness to TLR agonists, develop more Ly6C(hi)PDCA1(+) DCs that resemble inflammatory DCs and produce high levels of inflammatory cytokines. Also, compared with WT-infected mice, NOS2 KO mice infected with WNV showed enhanced expansion of a similar inflammatory Ly6C(hi)PDCA1(+) DC subset. Furthermore, in contrast to WT DCs, OVA-loaded NOS2 KO BM-DCs promoted increased IFN-γ production by OTII CD4(+) T cells in vitro and when adoptively transferred in vivo. The addition of a NO donor to NOS2 KO BM-DCs prior to OTII T cells priming in vivo was sufficient to revert Th1 immune responses to levels induced by WT BM-DCs. Thus, autocrine NO effects on maturation of inflammatory DCs and on DC programming of T cells may contribute to the protective role of NO in autoimmune diseases and infections. Regulating NO levels may be a useful tool to shape beneficial immune responses for DC-based immunotherapy.
    MeSH term(s) Animals ; Antigens, Ly/metabolism ; Antigens, Surface/metabolism ; Apoptosis Regulatory Proteins/metabolism ; B7-2 Antigen/metabolism ; Biomarkers/metabolism ; CD4-Positive T-Lymphocytes/immunology ; Cell Proliferation ; Cell Survival ; Cells, Cultured ; Cytokines/biosynthesis ; Dendritic Cells/enzymology ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Down-Regulation ; Epitopes/immunology ; Immunity/immunology ; Inflammation/immunology ; Inflammation/pathology ; Inflammation Mediators/metabolism ; Interferon-gamma/biosynthesis ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type II/deficiency ; Nitric Oxide Synthase Type II/metabolism ; Programmed Cell Death 1 Receptor ; Th1 Cells/immunology ; Toll-Like Receptors/immunology ; Up-Regulation ; West Nile Fever/immunology ; West Nile Fever/virology ; West Nile virus/physiology
    Chemical Substances Antigens, Ly ; Antigens, Surface ; Apoptosis Regulatory Proteins ; B7-2 Antigen ; Biomarkers ; Cytokines ; Epitopes ; Inflammation Mediators ; Ly-6C antigen, mouse ; Pdcd1 protein, mouse ; Programmed Cell Death 1 Receptor ; Toll-Like Receptors ; Nitric Oxide (31C4KY9ESH) ; Interferon-gamma (82115-62-6) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Nos2 protein, mouse (EC 1.14.13.39)
    Language English
    Publishing date 2010-12-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 605722-6
    ISSN 1938-3673 ; 0741-5400
    ISSN (online) 1938-3673
    ISSN 0741-5400
    DOI 10.1189/jlb.0610329
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 603: 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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  7. Article ; Online: IPS-1 is essential for the control of West Nile virus infection and immunity.

    Suthar, Mehul S / Ma, Daphne Y / Thomas, Sunil / Lund, Jennifer M / Zhang, Nu / Daffis, Stephane / Rudensky, Alexander Y / Bevan, Michael J / Clark, Edward A / Kaja, Murali-Krishna / Diamond, Michael S / Gale, Michael

    PLoS pathogens

    2010  Volume 6, Issue 2, Page(s) e1000757

    Abstract: The innate immune response is essential for controlling West Nile virus (WNV) infection but how this response is propagated and regulates adaptive immunity in vivo are not defined. Herein, we show that IPS-1, the central adaptor protein to RIG-I-like ... ...

    Abstract The innate immune response is essential for controlling West Nile virus (WNV) infection but how this response is propagated and regulates adaptive immunity in vivo are not defined. Herein, we show that IPS-1, the central adaptor protein to RIG-I-like receptor (RLR) signaling, is essential for triggering of innate immunity and for effective development and regulation of adaptive immunity against pathogenic WNV. IPS-1(-/-) mice exhibited increased susceptibility to WNV infection marked by enhanced viral replication and dissemination with early viral entry into the CNS. Infection of cultured bone-marrow (BM) derived dendritic cells (DCs), macrophages (Macs), and primary cortical neurons showed that the IPS-1-dependent RLR signaling was essential for triggering IFN defenses and controlling virus replication in these key target cells of infection. Intriguingly, infected IPS-1(-/-) mice displayed uncontrolled inflammation that included elevated systemic type I IFN, proinflammatory cytokine and chemokine responses, increased numbers of inflammatory DCs, enhanced humoral responses marked by complete loss of virus neutralization activity, and increased numbers of virus-specific CD8+ T cells and non-specific immune cell proliferation in the periphery and in the CNS. This uncontrolled inflammatory response was associated with a lack of regulatory T cell expansion that normally occurs during acute WNV infection. Thus, the enhanced inflammatory response in the absence of IPS-1 was coupled with a failure to protect against WNV infection. Our data define an innate/adaptive immune interface mediated through IPS-1-dependent RLR signaling that regulates the quantity, quality, and balance of the immune response to WNV infection.
    MeSH term(s) Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/immunology ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Antibodies, Viral/blood ; Blotting, Western ; Brain/immunology ; Brain/virology ; Cell Separation ; Cytokines/blood ; Cytokines/immunology ; DEAD Box Protein 58 ; DEAD-box RNA Helicases/genetics ; DEAD-box RNA Helicases/immunology ; DEAD-box RNA Helicases/metabolism ; Enzyme-Linked Immunosorbent Assay ; Flow Cytometry ; Gene Expression ; Immunity, Cellular/immunology ; Inflammation/immunology ; Mice ; Mice, Knockout ; Neurons/immunology ; Neurons/virology ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction/immunology ; West Nile Fever/genetics ; West Nile Fever/immunology ; West Nile Fever/metabolism ; West Nile virus/immunology
    Chemical Substances Adaptor Proteins, Signal Transducing ; Antibodies, Viral ; Cytokines ; IPS-1 protein, mouse ; Ddx58 protein, mouse (EC 3.6.1.-) ; DEAD Box Protein 58 (EC 3.6.4.13) ; DEAD-box RNA Helicases (EC 3.6.4.13)
    Keywords covid19
    Language English
    Publishing date 2010-02-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2205412-1
    ISSN 1553-7374 ; 1553-7366
    ISSN (online) 1553-7374
    ISSN 1553-7366
    DOI 10.1371/journal.ppat.1000757
    Database MEDical Literature Analysis and Retrieval System OnLINE

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