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  1. Article ; Online: Recent advances in the understanding of Nipah virus immunopathogenesis and anti-viral approaches.

    Pelissier, Rodolphe / Iampietro, Mathieu / Horvat, Branka

    F1000Research

    2019  Volume 8

    Abstract: Nipah virus (NiV) is a highly lethal zoonotic paramyxovirus that emerged at the end of last century as a human pathogen capable of causing severe acute respiratory infection and encephalitis. Although NiV provokes serious diseases in numerous mammalian ... ...

    Abstract Nipah virus (NiV) is a highly lethal zoonotic paramyxovirus that emerged at the end of last century as a human pathogen capable of causing severe acute respiratory infection and encephalitis. Although NiV provokes serious diseases in numerous mammalian species, the infection seems to be asymptomatic in NiV natural hosts, the fruit bats, which provide a continuous virus source for further outbreaks. Consecutive human-to-human transmission has been frequently observed during outbreaks in Bangladesh and India. NiV was shown to interfere with the innate immune response and interferon type I signaling, restraining the anti-viral response and permitting viral spread. Studies of adaptive immunity in infected patients and animal models have suggested an unbalanced immune response during NiV infection. Here, we summarize some of the recent studies of NiV pathogenesis and NiV-induced modulation of both innate and adaptive immune responses, as well as the development of novel prophylactic and therapeutic approaches, necessary to control this highly lethal emerging infection.
    MeSH term(s) Adaptive Immunity ; Animals ; Bangladesh ; Henipavirus Infections/immunology ; Humans ; Immunity, Innate ; India ; Nipah Virus/immunology ; Nipah Virus/pathogenicity
    Language English
    Publishing date 2019-10-16
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2699932-8
    ISSN 2046-1402 ; 2046-1402
    ISSN (online) 2046-1402
    ISSN 2046-1402
    DOI 10.12688/f1000research.19975.1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Diversité génomique virale : évaluation et conséquences sur la virulence des infections respiratoires.

    Pichon, Maxime / Pelissier, Rodolphe / Valette, Martine / Lina, Bruno / Josset, Laurence

    Virologie (Montrouge, France)

    2020  Volume 22, Issue 3, Page(s) 173–182

    Abstract: During host infection, viral replication generates multiple subpopulations. Studies of viral diversity using high-throughput sequencing technologies provide a better understanding of the therapeutic effects as well as of the viral pathogenesis. This ... ...

    Title translation Viral genomic diversity: Characterization and consequences on respiratory infections virulence.
    Abstract During host infection, viral replication generates multiple subpopulations. Studies of viral diversity using high-throughput sequencing technologies provide a better understanding of the therapeutic effects as well as of the viral pathogenesis. This technical evolution led to an impressive number of studies analyzing this viral characteristic. In this review, we will discuss the principles of the evaluation of viral diversity, before summarizing the main physiological consequences for respiratory viruses. To date, although no study clearly established its role in pathogenesis of severe forms, viral diversification can be alternately a formidable virulence advantage or deleterious to the virus, resulting in its extinction (error-threshold). Because of these differences, it is important to study it in the context of respiratory virus infection, such as Influenza, respiratory syncitial virus (RVS) or rhinovirus. The precise understanding of this property allows us to consider multiple clinical applications, i.e. therapeutic or preventive.
    Language French
    Publishing date 2020-10-28
    Publishing country France
    Document type Journal Article
    ZDB-ID 2118387-9
    ISSN 1950-6961 ; 1267-8694
    ISSN (online) 1950-6961
    ISSN 1267-8694
    DOI 10.1684/vir.2018.0738
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: STLV-1 Commonly Targets Neurons in the Brain of Asymptomatic Non-Human Primates.

    Rocamonde, Brenda / Alais, Sandrine / Pelissier, Rodolphe / Moulin, Valerie / Rimbaud, Brigitte / Lacoste, Romain / Aurine, Noemie / Baquerre, Camille / Pain, Bertrand / Tanaka, Yuetsu / Mathieu, Cyrille / Dutartre, Hélène

    mBio

    2023  Volume 14, Issue 2, Page(s) e0352622

    Abstract: The human T-cell leukemia virus (HTLV)-1 is responsible for an aggressive neurodegenerative disease (HAM/TSP) and multiple neurological alterations. The capacity of HTLV-1 to infect central nervous system (CNS) resident cells, together with the ... ...

    Abstract The human T-cell leukemia virus (HTLV)-1 is responsible for an aggressive neurodegenerative disease (HAM/TSP) and multiple neurological alterations. The capacity of HTLV-1 to infect central nervous system (CNS) resident cells, together with the neuroimmune-driven response, has not been well-established. Here, we combined the use of human induced pluripotent stem cells (hiPSC) and of naturally STLV-1-infected nonhuman primates (NHP) as models with which to investigate HTLV-1 neurotropism. Hence, neuronal cells obtained after hiPSC differentiation in neural polycultures were the main cell population infected by HTLV-1. Further, we report the infection of neurons with STLV-1 in spinal cord regions as well as in brain cortical and cerebellar sections of postmortem NHP. Additionally, reactive microglial cells were found in infected areas, suggesting an immune antiviral response. These results emphasize the need to develop new efficient models by which to understand HTLV-1 neuroinfection and suggest an alternative mechanism that leads to HAM/TSP.
    MeSH term(s) Animals ; Humans ; Simian T-lymphotropic virus 1 ; Neurodegenerative Diseases ; Induced Pluripotent Stem Cells ; Brain ; Human T-lymphotropic virus 1/physiology ; Primates ; Neurons
    Language English
    Publishing date 2023-02-21
    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.03526-22
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Nipah virus W protein harnesses nuclear 14-3-3 to inhibit NF-κB-induced proinflammatory response.

    Enchéry, François / Dumont, Claire / Iampietro, Mathieu / Pelissier, Rodolphe / Aurine, Noémie / Bloyet, Louis-Marie / Carbonnelle, Caroline / Mathieu, Cyrille / Journo, Chloé / Gerlier, Denis / Horvat, Branka

    Communications biology

    2021  Volume 4, Issue 1, Page(s) 1292

    Abstract: Nipah virus (NiV) is a highly pathogenic emerging bat-borne Henipavirus that has caused numerous outbreaks with public health concerns. It is able to inhibit the host innate immune response. Since the NF-κB pathway plays a crucial role in the innate ... ...

    Abstract Nipah virus (NiV) is a highly pathogenic emerging bat-borne Henipavirus that has caused numerous outbreaks with public health concerns. It is able to inhibit the host innate immune response. Since the NF-κB pathway plays a crucial role in the innate antiviral response as a major transcriptional regulator of inflammation, we postulated its implication in the still poorly understood NiV immunopathogenesis. We report here that NiV inhibits the canonical NF-κB pathway via its nonstructural W protein. Translocation of the W protein into the nucleus causes nuclear accumulation of the cellular scaffold protein 14-3-3 in both African green monkey and human cells infected by NiV. Excess of 14-3-3 in the nucleus was associated with a reduction of NF-κB p65 subunit phosphorylation and of its nuclear accumulation. Importantly, W-S449A substitution impairs the binding of the W protein to 14-3-3 and the subsequent suppression of NF-κB signaling, thus restoring the production of proinflammatory cytokines. Our data suggest that the W protein increases the steady-state level of 14-3-3 in the nucleus and consequently enhances 14-3-3-mediated negative feedback on the NF-κB pathway. These findings provide a mechanistic model of W-mediated disruption of the host inflammatory response, which could contribute to the high severity of NiV infection.
    MeSH term(s) Animals ; Cell Line ; Cell Nucleus/immunology ; Chlorocebus aethiops ; HEK293 Cells ; HeLa Cells ; Humans ; Immunity, Innate/physiology ; NF-kappa B ; Nipah Virus/genetics ; Nipah Virus/physiology ; Signal Transduction/immunology ; Viral Proteins/metabolism
    Chemical Substances NF-kappa B ; Viral Proteins ; W protein, Nipah virus
    Language English
    Publishing date 2021-11-16
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2399-3642
    ISSN (online) 2399-3642
    DOI 10.1038/s42003-021-02797-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Hamster organotypic modeling of SARS-CoV-2 lung and brainstem infection.

    Ferren, Marion / Favède, Valérie / Decimo, Didier / Iampietro, Mathieu / Lieberman, Nicole A P / Weickert, Jean-Luc / Pelissier, Rodolphe / Mazelier, Magalie / Terrier, Olivier / Moscona, Anne / Porotto, Matteo / Greninger, Alexander L / Messaddeq, Nadia / Horvat, Branka / Mathieu, Cyrille

    Nature communications

    2021  Volume 12, Issue 1, Page(s) 5809

    Abstract: SARS-CoV-2 has caused a global pandemic of COVID-19 since its emergence in December 2019. The infection causes a severe acute respiratory syndrome and may also spread to central nervous system leading to neurological sequelae. We have developed and ... ...

    Abstract SARS-CoV-2 has caused a global pandemic of COVID-19 since its emergence in December 2019. The infection causes a severe acute respiratory syndrome and may also spread to central nervous system leading to neurological sequelae. We have developed and characterized two new organotypic cultures from hamster brainstem and lung tissues that offer a unique opportunity to study the early steps of viral infection and screening antivirals. These models are not dedicated to investigate how the virus reaches the brain. However, they allow validating the early tropism of the virus in the lungs and demonstrating that SARS-CoV-2 could infect the brainstem and the cerebellum, mainly by targeting granular neurons. Viral infection induces specific interferon and innate immune responses with patterns specific to each organ, along with cell death by apoptosis, necroptosis, and pyroptosis. Overall, our data illustrate the potential of rapid modeling of complex tissue-level interactions during infection by a newly emerged virus.
    MeSH term(s) Adenosine Monophosphate/analogs & derivatives ; Adenosine Monophosphate/pharmacology ; Alanine/analogs & derivatives ; Alanine/pharmacology ; Alveolar Epithelial Cells/virology ; Animals ; Antiviral Agents/pharmacology ; Brain Stem/cytology ; Brain Stem/immunology ; Brain Stem/pathology ; Brain Stem/virology ; Cricetinae ; Immunity, Innate ; Inflammation ; Lung/cytology ; Lung/immunology ; Lung/pathology ; Lung/virology ; Models, Biological ; Neurons/virology ; Organ Culture Techniques ; Regulated Cell Death ; SARS-CoV-2/drug effects ; SARS-CoV-2/pathogenicity ; Viral Tropism
    Chemical Substances Antiviral Agents ; remdesivir (3QKI37EEHE) ; Adenosine Monophosphate (415SHH325A) ; Alanine (OF5P57N2ZX)
    Language English
    Publishing date 2021-10-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-021-26096-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Activation of cGAS/STING pathway upon paramyxovirus infection.

    Iampietro, Mathieu / Dumont, Claire / Mathieu, Cyrille / Spanier, Julia / Robert, Jonathan / Charpenay, Aude / Dupichaud, Sébastien / Dhondt, Kévin P / Aurine, Noémie / Pelissier, Rodolphe / Ferren, Marion / Mély, Stéphane / Gerlier, Denis / Kalinke, Ulrich / Horvat, Branka

    iScience

    2021  Volume 24, Issue 6, Page(s) 102519

    Abstract: During inflammatory diseases, cancer, and infection, the cGAS/STING pathway is known to recognize foreign or self-DNA in the cytosol and activate an innate immune response. Here, we report that negative-strand RNA paramyxoviruses, Nipah virus (NiV), and ... ...

    Abstract During inflammatory diseases, cancer, and infection, the cGAS/STING pathway is known to recognize foreign or self-DNA in the cytosol and activate an innate immune response. Here, we report that negative-strand RNA paramyxoviruses, Nipah virus (NiV), and measles virus (MeV), can also trigger the cGAS/STING axis. Although mice deficient for MyD88, TRIF, and MAVS still moderately control NiV infection when compared with wild-type mice, additional STING deficiency resulted in 100% lethality, suggesting synergistic roles of these pathways in host protection. Moreover, deletion of cGAS or STING resulted in decreased type I interferon production with enhanced paramyxoviral infection in both human and murine cells. Finally, the phosphorylation and ubiquitination of STING, observed during viral infections, confirmed the activation of cGAS/STING pathway by NiV and MeV. Our data suggest that cGAS/STING activation is critical in controlling paramyxovirus infection and possibly represents attractive targets to develop countermeasures against severe disease induced by these pathogens.
    Language English
    Publishing date 2021-05-07
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2021.102519
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Control of Nipah Virus Infection in Mice by the Host Adaptors Mitochondrial Antiviral Signaling Protein (MAVS) and Myeloid Differentiation Primary Response 88 (MyD88).

    Iampietro, Mathieu / Aurine, Noemie / Dhondt, Kevin P / Dumont, Claire / Pelissier, Rodolphe / Spanier, Julia / Vallve, Audrey / Raoul, Herve / Kalinke, Ulrich / Horvat, Branka

    The Journal of infectious diseases

    2019  Volume 221, Issue Suppl 4, Page(s) S401–S406

    Abstract: Interferon (IFN) type I plays a critical role in the protection of mice from lethal Nipah virus (NiV) infection, but mechanisms responsible for IFN-I induction remain unknown. In the current study, we demonstrated the critical role of the mitochondrial ... ...

    Abstract Interferon (IFN) type I plays a critical role in the protection of mice from lethal Nipah virus (NiV) infection, but mechanisms responsible for IFN-I induction remain unknown. In the current study, we demonstrated the critical role of the mitochondrial antiviral signaling protein signaling pathway in IFN-I production and NiV replication in murine embryonic fibroblasts in vitro, and the redundant but essential roles of both mitochondrial antiviral signaling protein and myeloid differentiation primary response 88 adaptors, but not toll/interleukin-1 receptor/resistance [TIR] domain-containing adaptor-inducing IFN-β (TRIF), in the control of NiV infection in mice. These results reveal potential novel targets for antiviral intervention and help in understanding NiV immunopathogenesis.
    MeSH term(s) Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; DEAD Box Protein 58/genetics ; DEAD Box Protein 58/metabolism ; Gene Expression Regulation/immunology ; Henipavirus Infections/immunology ; Henipavirus Infections/virology ; Interferon Type I/genetics ; Interferon Type I/metabolism ; Interferon-beta/genetics ; Interferon-beta/metabolism ; Mice ; Mice, Knockout ; Mice, Transgenic ; Myeloid Differentiation Factor 88/genetics ; Myeloid Differentiation Factor 88/metabolism ; Nipah Virus ; Toll-Like Receptors/genetics ; Toll-Like Receptors/metabolism
    Chemical Substances Adaptor Proteins, Signal Transducing ; IPS-1 protein, mouse ; Interferon Type I ; Myd88 protein, mouse ; Myeloid Differentiation Factor 88 ; Toll-Like Receptors ; VISA protein, mouse ; Interferon-beta (77238-31-4) ; Ddx58 protein, mouse (EC 3.6.1.-) ; DEAD Box Protein 58 (EC 3.6.4.13)
    Language English
    Publishing date 2019-12-18
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3019-3
    ISSN 1537-6613 ; 0022-1899
    ISSN (online) 1537-6613
    ISSN 0022-1899
    DOI 10.1093/infdis/jiz602
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Control of Nipah Virus Infection in Mice by the Host Adaptors Mitochondrial Antiviral Signaling Protein (MAVS) and Myeloid Differentiation Primary Response 88 (MyD88).

    Iampietro, Mathieu / Aurine, Noemie / Dhondt, Kevin P / Dumont, Claire / Pelissier, Rodolphe / Spanier, Julia / Vallve, Audrey / Raoul, Herve / Kalinke, Ulrich / Horvat, Branka

    The Journal of infectious diseases

    2019  

    Abstract: Interferon (IFN) type I plays a critical role in the protection of mice from lethal Nipah virus (NiV) infection, but mechanisms responsible for IFN-I induction remain unknown. In the current study, we demonstrated the critical role of the mitochondrial ... ...

    Abstract Interferon (IFN) type I plays a critical role in the protection of mice from lethal Nipah virus (NiV) infection, but mechanisms responsible for IFN-I induction remain unknown. In the current study, we demonstrated the critical role of the mitochondrial antiviral signaling protein signaling pathway in IFN-I production and NiV replication in murine embryonic fibroblasts in vitro, and the redundant but essential roles of both mitochondrial antiviral signaling protein and myeloid differentiation primary response 88 adaptors, but not TRIF (Toll/Interleukin-1 receptor/Resistance [TIR] domain-containing adaptor-inducing IFN-β), in the control of NiV infection in mice. These results reveal potential novel targets for antiviral intervention and help in understanding NiV immunopathogenesis.
    Keywords MAVS ; MyD88 ; Nipah virus ; TLR ; TRIF ; innate immunity ; interferon ; mice
    Subject code 570
    Language English
    Publishing date 2019-12-19
    Publisher Oxford Academic
    Publishing country de
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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