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  1. Article ; Online: Mechanisms of severe acute respiratory syndrome pathogenesis and innate immunomodulation.

    Frieman, Matthew / Baric, Ralph

    Microbiology and molecular biology reviews : MMBR

    2008  Volume 72, Issue 4, Page(s) 672–85, Table of Contents

    Abstract: ... The emergence of the highly pathogenic coronavirus severe acute respiratory virus (SARS-CoV) serves as a robust ... suggesting the possibility of novel strategies for targeting and regulating host innate ... in humans and animals. Coronaviruses encode the largest positive-sense RNA genome of approximately 30 kb ...

    Abstract The modulation of the immune response is a common practice of many highly pathogenic viruses. The emergence of the highly pathogenic coronavirus severe acute respiratory virus (SARS-CoV) serves as a robust model system to elucidate the virus-host interactions that mediate severe end-stage lung disease in humans and animals. Coronaviruses encode the largest positive-sense RNA genome of approximately 30 kb, encode a variety of replicase and accessory open reading frames that are structurally unique, and encode novel enzymatic functions among RNA viruses. These viruses have broad or specific host ranges, suggesting the possibility of novel strategies for targeting and regulating host innate immune responses following virus infection. Using SARS-CoV as a model, we review the current literature on the ability of coronaviruses to interact with and modify the host intracellular environment during infection. These studies are revealing a rich set of novel viral proteins that engage, modify, and/or disrupt host cell signaling and nuclear import machinery for the benefit of virus replication.
    MeSH term(s) Animals ; Coronavirus/genetics ; Coronavirus/physiology ; Coronavirus Infections/virology ; Genome, Viral/genetics ; Humans ; Immunity, Innate ; Severe acute respiratory syndrome-related coronavirus/genetics ; Severe acute respiratory syndrome-related coronavirus/immunology ; Severe acute respiratory syndrome-related coronavirus/pathogenicity ; Severe Acute Respiratory Syndrome/genetics ; Severe Acute Respiratory Syndrome/immunology ; Severe Acute Respiratory Syndrome/virology ; Virus Replication
    Keywords covid19
    Language English
    Publishing date 2008-11-28
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1376131-6
    ISSN 1098-5557 ; 1070-6275 ; 1092-2172
    ISSN (online) 1098-5557 ; 1070-6275
    ISSN 1092-2172
    DOI 10.1128/MMBR.00015-08
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Endothelial dysfunction and immunothrombosis as key pathogenic mechanisms in COVID-19.

    Bonaventura, Aldo / Vecchié, Alessandra / Dagna, Lorenzo / Martinod, Kimberly / Dixon, Dave L / Van Tassell, Benjamin W / Dentali, Francesco / Montecucco, Fabrizio / Massberg, Steffen / Levi, Marcel / Abbate, Antonio

    Nature reviews. Immunology

    2021  Volume 21, Issue 5, Page(s) 319–329

    Abstract: ... complications may contribute to acute respiratory distress syndrome (ARDS) and other organ dysfunctions ... with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Patients with severe disease show hyperactivation of the immune system ... its complications may help to improve risk stratification and develop targeted therapies to reduce the acute and ...

    Abstract Coronavirus disease 2019 (COVID-19) is a clinical syndrome caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Patients with severe disease show hyperactivation of the immune system, which can affect multiple organs besides the lungs. Here, we propose that SARS-CoV-2 infection induces a process known as immunothrombosis, in which activated neutrophils and monocytes interact with platelets and the coagulation cascade, leading to intravascular clot formation in small and larger vessels. Microthrombotic complications may contribute to acute respiratory distress syndrome (ARDS) and other organ dysfunctions. Therapeutic strategies aimed at reducing immunothrombosis may therefore be useful. Several antithrombotic and immunomodulating drugs have been proposed as candidates to treat patients with SARS-CoV-2 infection. The growing understanding of SARS-CoV-2 infection pathogenesis and how it contributes to critical illness and its complications may help to improve risk stratification and develop targeted therapies to reduce the acute and long-term consequences of this disease.
    MeSH term(s) Blood Coagulation/immunology ; Blood Platelets/immunology ; COVID-19/immunology ; COVID-19/pathology ; Critical Illness/therapy ; Cytokine Release Syndrome/immunology ; Cytokine Release Syndrome/pathology ; Endothelium, Vascular/pathology ; Fibrinolytic Agents/therapeutic use ; Humans ; Immunity, Innate/immunology ; Lung/blood supply ; Lung/pathology ; Lung/virology ; Monocytes/immunology ; Neutrophils/immunology ; SARS-CoV-2/immunology ; SARS-CoV-2/pathogenicity ; Venous Thrombosis/immunology ; Venous Thrombosis/pathology ; Venous Thrombosis/prevention & control
    Chemical Substances Fibrinolytic Agents
    Language English
    Publishing date 2021-04-06
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2062776-2
    ISSN 1474-1741 ; 1474-1733
    ISSN (online) 1474-1741
    ISSN 1474-1733
    DOI 10.1038/s41577-021-00536-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Report of the 'mechanisms of lung injury and immunomodulator interventions in influenza' workshop, 21 March 2010, Ventura, California, USA.

    Howard, Wendy A / Peiris, Malik / Hayden, Frederick G

    Influenza and other respiratory viruses

    2011  Volume 5, Issue 6, Page(s) 453–4, e458–75

    Abstract: ... of lung injury in acute influenza and describe cellular and molecular mechanisms of lung injury that are common ... distress syndrome (ARDS) is the principal cause of respiratory failure associated with severe influenza ... exuberant or dysregulated innate inflammatory responses or sometimes deficient responses. Acute respiratory ...

    Abstract The clinical course of influenza and the extent of lung injury are determined by both viral and host factors, as well as sometimes secondary bacterial infections and exacerbations of underlying conditions. The balance between viral replication and the host immune responses is central to disease pathogenesis, and the extent of lung injury in severe influenza infections may be due in part to overly exuberant or dysregulated innate inflammatory responses or sometimes deficient responses. Acute respiratory distress syndrome (ARDS) is the principal cause of respiratory failure associated with severe influenza. ARDS can be triggered by both direct lung insults (e.g. respiratory pathogens) and systemic insults (e.g. sepsis), and the lung damage is exacerbated by the inflammatory response associated with either infectious or non-infectious insults. This workshop aimed to review the current understanding of lung injury in acute influenza and describe cellular and molecular mechanisms of lung injury that are common to influenza and infections by other respiratory pathogens. In addition, therapeutic agents that target host response proteins and pathways were identified and investigational agents in development reviewed. A logical strategy would be to combine antiviral treatment with drugs that modify excessive host responses or supplement deficient ones. However, a better understanding of common cell signalling pathways associated with acute lung injury caused by influenza and other pathogens is necessary to understand immunopathologic causes of lung injury. This will help determine which immunomodulatory interventions might be useful, and to predict the appropriate timing and consequences of their use.
    MeSH term(s) Animals ; Humans ; Immunologic Factors/therapeutic use ; Influenza A Virus, H1N1 Subtype/genetics ; Influenza A Virus, H1N1 Subtype/immunology ; Influenza A Virus, H1N1 Subtype/physiology ; Influenza A Virus, H5N1 Subtype/genetics ; Influenza A Virus, H5N1 Subtype/immunology ; Influenza A Virus, H5N1 Subtype/physiology ; Influenza, Human/complications ; Influenza, Human/immunology ; Influenza, Human/virology ; Lung Injury/drug therapy ; Lung Injury/etiology ; Lung Injury/immunology
    Chemical Substances Immunologic Factors
    Keywords covid19
    Language English
    Publishing date 2011-08-17
    Publishing country England
    Document type Congress ; Research Support, Non-U.S. Gov't
    ZDB-ID 2274538-5
    ISSN 1750-2659 ; 1750-2640
    ISSN (online) 1750-2659
    ISSN 1750-2640
    DOI 10.1111/j.1750-2659.2011.00278.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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