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  1. Article ; Online: Interplay between RNA viruses and cGAS/STING axis in innate immunity.

    Amurri, Lucia / Horvat, Branka / Iampietro, Mathieu

    Frontiers in cellular and infection microbiology

    2023  Volume 13, Page(s) 1172739

    Abstract: While the function of cGAS/STING signalling axis in the innate immune response to DNA viruses is well deciphered, increasing evidence demonstrates its significant contribution in the control of RNA virus infections. After the first evidence of cGAS/STING ...

    Abstract While the function of cGAS/STING signalling axis in the innate immune response to DNA viruses is well deciphered, increasing evidence demonstrates its significant contribution in the control of RNA virus infections. After the first evidence of cGAS/STING antagonism by flaviviruses, STING activation has been detected following infection by various enveloped RNA viruses. It has been discovered that numerous viral families have implemented advanced strategies to antagonize STING pathway through their evolutionary path. This review summarizes the characterized cGAS/STING escape strategies to date, together with the proposed mechanisms of STING signalling activation perpetrated by RNA viruses and discusses possible therapeutic approaches. Further studies regarding the interaction between RNA viruses and cGAS/STING-mediated immunity could lead to major discoveries important for the understanding of immunopathogenesis and for the treatment of RNA viral infections.
    MeSH term(s) Humans ; Immunity, Innate ; Nucleotidyltransferases/metabolism ; RNA Viruses ; Signal Transduction
    Chemical Substances Nucleotidyltransferases (EC 2.7.7.-)
    Language English
    Publishing date 2023-04-03
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2619676-1
    ISSN 2235-2988 ; 2235-2988
    ISSN (online) 2235-2988
    ISSN 2235-2988
    DOI 10.3389/fcimb.2023.1172739
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Mouse Models of Henipavirus Infection.

    Iampietro, Mathieu / Barron, Stéphane / Duthey, Aurélie / Horvat, Branka

    Methods in molecular biology (Clifton, N.J.)

    2023  Volume 2682, Page(s) 137–147

    Abstract: The Nipah and Hendra viruses, belonging to henipavirus genus, are recently emerged zoonotic pathogens that cause severe and often fatal, neurologic, and/or respiratory diseases in both humans and various animals. As mice represent a small animal model ... ...

    Abstract The Nipah and Hendra viruses, belonging to henipavirus genus, are recently emerged zoonotic pathogens that cause severe and often fatal, neurologic, and/or respiratory diseases in both humans and various animals. As mice represent a small animal model convenient to study viral infections and provide a well-developed experimental toolbox for analysis in immunovirology, we describe in this chapter a few basic methods used in biosafety 4 level (BSL4) conditions to study henipavirus infection in mice.
    MeSH term(s) Humans ; Animals ; Mice ; Henipavirus Infections ; Disease Models, Animal
    Language English
    Publishing date 2023-08-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-3283-3_10
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Interplay of Ebola Virus With Immune Cells Leading to Their Death by Diverse Mechanisms.

    Iampietro, Mathieu / Amurri, Lucia / Reynard, Olivier / Bukreyev, Alexander

    The Journal of infectious diseases

    2023  Volume 228, Issue Suppl 7, Page(s) S582–S586

    Abstract: Inflammation and cytopenia are commonly observed during Ebola virus (EBOV) infection; however, mechanisms responsible for EBOV-induced cell death remain obscure. While apoptosis and necrosis are already identified as mechanisms of cell death induced by ... ...

    Abstract Inflammation and cytopenia are commonly observed during Ebola virus (EBOV) infection; however, mechanisms responsible for EBOV-induced cell death remain obscure. While apoptosis and necrosis are already identified as mechanisms of cell death induced by the virus, our study demonstrates that THP-1 monocytes and SupT1 T cells exposed to EBOV undergo pyroptosis and necroptosis, respectively, through a direct contact with EBOV, and also mediate pyroptosis or necroptosis of uninfected bystander cells via indirect effects associated with secreted soluble factors. These results emphasize novel aspects of interactions between EBOV and immune cell populations and provide a better understanding of the immunopathogenesis of EBOV disease.
    MeSH term(s) Humans ; Ebolavirus ; Hemorrhagic Fever, Ebola ; T-Lymphocytes/metabolism ; Apoptosis ; Cell Death
    Language English
    Publishing date 2023-08-31
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 3019-3
    ISSN 1537-6613 ; 0022-1899
    ISSN (online) 1537-6613
    ISSN 0022-1899
    DOI 10.1093/infdis/jiad377
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: La voie de signalisation cGAS/STING contrôle les infections par le virus de la rougeole et par le virus Nipah.

    Iampietro, Mathieu / Amurri, Lucia / Horvat, Branka

    Medecine sciences : M/S

    2022  Volume 38, Issue 4, Page(s) 339–342

    Title translation The cGAS/STING signaling pathway controls infections by measles and Nipah viruses.
    MeSH term(s) Humans ; Measles/epidemiology ; Nipah Virus/metabolism ; Nucleotidyltransferases ; Signal Transduction
    Chemical Substances Nucleotidyltransferases (EC 2.7.7.-)
    Language French
    Publishing date 2022-04-29
    Publishing country France
    Document type Journal Article
    ZDB-ID 632733-3
    ISSN 1958-5381 ; 0767-0974
    ISSN (online) 1958-5381
    ISSN 0767-0974
    DOI 10.1051/medsci/2022036
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Measles Virus-Induced Host Immunity and Mechanisms of Viral Evasion.

    Amurri, Lucia / Reynard, Olivier / Gerlier, Denis / Horvat, Branka / Iampietro, Mathieu

    Viruses

    2022  Volume 14, Issue 12

    Abstract: The immune system deploys a complex network of cells and signaling pathways to protect host integrity against exogenous threats, including measles virus (MeV). However, throughout its evolutionary path, MeV developed various mechanisms to disrupt and ... ...

    Abstract The immune system deploys a complex network of cells and signaling pathways to protect host integrity against exogenous threats, including measles virus (MeV). However, throughout its evolutionary path, MeV developed various mechanisms to disrupt and evade immune responses. Despite an available vaccine, MeV remains an important re-emerging pathogen with a continuous increase in prevalence worldwide during the last decade. Considerable knowledge has been accumulated regarding MeV interactions with the innate immune system through two antagonistic aspects: recognition of the virus by cellular sensors and viral ability to inhibit the induction of the interferon cascade. Indeed, while the host could use several innate adaptors to sense MeV infection, the virus is adapted to unsettle defenses by obstructing host cell signaling pathways. Recent works have highlighted a novel aspect of innate immune response directed against MeV unexpectedly involving DNA-related sensing through activation of the cGAS/STING axis, even in the absence of any viral DNA intermediate. In addition, while MeV infection most often causes a mild disease and triggers a lifelong immunity, its tropism for invariant T-cells and memory T and B-cells provokes the elimination of one primary shield and the pre-existing immunity against previously encountered pathogens, known as "immune amnesia".
    MeSH term(s) Humans ; Immune Evasion ; Immunity, Innate ; Interferons ; Measles/immunology ; Measles virus ; Signal Transduction
    Chemical Substances Interferons (9008-11-1)
    Language English
    Publishing date 2022-11-26
    Publishing country Switzerland
    Document type Journal Article ; Review ; 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/v14122641
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Early Permissiveness of Central Nervous System Cells to Measles Virus Infection Is Determined by Hyperfusogenicity and Interferon Pressure.

    Ferren, Marion / Lalande, Alexandre / Iampietro, Mathieu / Canus, Lola / Decimo, Didier / Gerlier, Denis / Porotto, Matteo / Mathieu, Cyrille

    Viruses

    2023  Volume 15, Issue 1

    Abstract: The cessation of measles virus (MeV) vaccination in more than 40 countries as a consequence of the COVID-19 pandemic is expected to significantly increase deaths due to measles. MeV can infect the central nervous system (CNS) and lead to lethal ... ...

    Abstract The cessation of measles virus (MeV) vaccination in more than 40 countries as a consequence of the COVID-19 pandemic is expected to significantly increase deaths due to measles. MeV can infect the central nervous system (CNS) and lead to lethal encephalitis. Substantial part of virus sequences recovered from patients' brain were mutated in the matrix and/or the fusion protein (F). Mutations of the heptad repeat domain located in the C terminal (HRC) part of the F protein were often observed and were associated to hyperfusogenicity. These mutations promote brain invasion as a hallmark of neuroadaptation. Wild-type F allows entry into the brain, followed by limited spreading compared with the massive invasion observed for hyperfusogenic MeV. Taking advantage of our ex vivo models of hamster organotypic brain cultures, we investigated how the hyperfusogenic mutations in the F HRC domain modulate virus distribution in CNS cells. In this study, we also identified the dependence of neural cells susceptibility on both their activation state and destabilization of the virus F protein. Type I interferon (IFN-I) impaired mainly astrocytes and microglial cells permissiveness contrarily to neurons, opening a new way of consideration on the development of treatments against viral encephalitis.
    MeSH term(s) Animals ; Cricetinae ; Humans ; Brain ; Central Nervous System/virology ; Interferons/metabolism ; Measles ; Measles virus/physiology ; Viral Fusion Proteins/genetics
    Chemical Substances Interferons (9008-11-1) ; Viral Fusion Proteins
    Language English
    Publishing date 2023-01-13
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; 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/v15010229
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. 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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  8. Article ; Online: Disabling of lymphocyte immune response by Ebola virus.

    Younan, Patrick / Iampietro, Mathieu / Bukreyev, Alexander

    PLoS pathogens

    2018  Volume 14, Issue 4, Page(s) e1006932

    MeSH term(s) Ebolavirus/immunology ; Hemorrhagic Fever, Ebola/complications ; Hemorrhagic Fever, Ebola/immunology ; Hemorrhagic Fever, Ebola/virology ; Humans ; Lymphocytes/immunology ; Lymphopenia/etiology
    Language English
    Publishing date 2018-04-12
    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.1006932
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  9. Article ; Online: Ebola Virus Shed Glycoprotein Triggers Differentiation, Infection, and Death of Monocytes Through Toll-Like Receptor 4 Activation.

    Iampietro, Mathieu / Santos, Rodrigo I / Lubaki, Ndongala Michel / Bukreyev, Alexander

    The Journal of infectious diseases

    2018  Volume 218, Issue suppl_5, Page(s) S327–S334

    Abstract: A better understanding of the mechanisms used by Ebola virus to disable the host immune system and spread the infection are of great importance for development of new therapeutic strategies. We demonstrate that treatment of monocytic cells with Ebola ... ...

    Abstract A better understanding of the mechanisms used by Ebola virus to disable the host immune system and spread the infection are of great importance for development of new therapeutic strategies. We demonstrate that treatment of monocytic cells with Ebola virus shed glycoprotein (GP) promotes their differentiation resulting in increased infection and cell death. The effects were inhibited by blocking Toll-like receptor 4 pathway. In addition, high levels of shed GP were detected in supernatants of cells treated with Ebola vaccines. This study highlights the role of shed GP in Ebola pathogenesis and also in adverse effects associated with Ebola vaccines.
    MeSH term(s) Cell Death/immunology ; Cell Death/physiology ; Cell Differentiation/immunology ; Cell Differentiation/physiology ; Ebola Vaccines/immunology ; Ebolavirus/immunology ; Ebolavirus/metabolism ; Glycoproteins/immunology ; Glycoproteins/metabolism ; Hemorrhagic Fever, Ebola/immunology ; Hemorrhagic Fever, Ebola/metabolism ; Hemorrhagic Fever, Ebola/virology ; Host-Pathogen Interactions/immunology ; Host-Pathogen Interactions/physiology ; Humans ; Monocytes/immunology ; Monocytes/metabolism ; Monocytes/physiology ; Monocytes/virology ; THP-1 Cells/metabolism ; THP-1 Cells/physiology ; THP-1 Cells/virology ; Toll-Like Receptor 4/metabolism ; Viral Envelope Proteins/metabolism
    Chemical Substances Ebola Vaccines ; Glycoproteins ; TLR4 protein, human ; Toll-Like Receptor 4 ; Viral Envelope Proteins
    Language English
    Publishing date 2018-08-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 3019-3
    ISSN 1537-6613 ; 0022-1899
    ISSN (online) 1537-6613
    ISSN 0022-1899
    DOI 10.1093/infdis/jiy406
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Hamster organotypic kidney culture model of early-stage SARS-CoV-2 infection highlights a two-step renal susceptibility.

    Shyfrin, Sophie R / Ferren, Marion / Perrin-Cocon, Laure / Espi, Maxime / Charmetant, Xavier / Brailly, Manon / Decimo, Didier / Iampietro, Mathieu / Canus, Lola / Horvat, Branka / Lotteau, Vincent / Vidalain, Pierre-Olivier / Thaunat, Olivier / Mathieu, Cyrille

    Journal of tissue engineering

    2022  Volume 13, Page(s) 20417314221122130

    Abstract: Kidney pathology is frequently reported in patients hospitalized with COVID-19, the pandemic disease caused by the Severe acute respiratory coronavirus 2 (SARS-CoV-2). However, due to a lack of suitable study models, the events occurring in the kidney ... ...

    Abstract Kidney pathology is frequently reported in patients hospitalized with COVID-19, the pandemic disease caused by the Severe acute respiratory coronavirus 2 (SARS-CoV-2). However, due to a lack of suitable study models, the events occurring in the kidney during the earliest stages of infection remain unknown. We have developed hamster organotypic kidney cultures (OKCs) to study the early stages of direct renal infection. OKCs maintained key renal structures in their native three-dimensional arrangement. SARS-CoV-2 productively replicated in hamster OKCs, initially targeting endothelial cells and later disseminating into proximal tubules. We observed a delayed interferon response, markers of necroptosis and pyroptosis, and an early repression of pro-inflammatory cytokines transcription followed by a strong later upregulation. While it remains an open question whether an active replication of SARS-CoV-2 takes place in the kidneys of COVID-19 patients with AKI, our model provides new insights into the kinetics of SARS-CoV-2 kidney infection and can serve as a powerful tool for studying kidney infection by other pathogens and testing the renal toxicity of drugs.
    Language English
    Publishing date 2022-09-06
    Publishing country England
    Document type Journal Article
    ZDB-ID 2573915-3
    ISSN 2041-7314
    ISSN 2041-7314
    DOI 10.1177/20417314221122130
    Database MEDical Literature Analysis and Retrieval System OnLINE

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