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Principal Investigator: Katrin Mayer-Barber
Organization: NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES
Fiscal Year: 2024
Award: $105,946
Funding agency: National Institute of Allergy and Infectious Diseases
The lungs of patients suffering from severe Coronavirus Disease 2019 (COVID-19) present with pneumonia and significant tissue damage which can lead to acute respiratory distress syndrome (ARDS) and death. This tissue destruction is caused not only by the etiological, cytopathic Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2) itself, but also a dysregulated host immune response. A phenomenon termed cytokine storm", which is characterized by high levels of pro-inflammatory cytokines such as IL-6 and IL-1, has been observed as a consequence of this dysregulated antiviral immunity. Understanding the complex host response to SARS-CoV-2 infection is a crucial global challenge. We leverage here our current expertise in inflammatory cytokines and pulmonary pathophysiology, operation in our high-containment (BSL3) research environment and importantly, animal BSL3 facilities, to investigate the host molecular and cellular mechanisms that contribute to pathogenesis during SARS-CoV-2 infection and importantly co-infection with other pulmonary pathogens. In particular, we will focus on the very earliest innate immune responses to to viral infection in the lung, with emphasis on how the inflammatory microenvironment of the lung impacts innate control of viral replication in the lung, prior to the onset of adaptive immunity.
Terms: <2019 novel corona virus><2019 novel coronavirus><2019-nCoV><ARDS><Acute Respiratory Distress><Acute Respiratory Distress Syndrome><Adult ARDS><Adult RDS><Adult Respiratory Distress Syndrome><Animal Model><Animal Models and Related Studies><Animals><B cell differentiation factor><B cell stimulating factor 2><B-Cell Differentiation Factor><B-Cell Differentiation Factor-2><B-Cell Stimulatory Factor-2><BCDF><BSF-2><BSF2><BSL-3 facility><BSL3 facility><Body Tissues><COVID-19 infection><COVID-19 virus><COVID-19 virus infection><COVID19 infection><COVID19 virus><Causality><Cause of Death><Cessation of life><CoV-2><CoV2><Complex><Containment><Da Nang Lung><Death><Dysfunction><Environment><Etiology><Functional disorder><HPGF><Hepatocyte-Stimulating Factor><Hybridoma Growth Factor><IFN-beta 2><IFNB2><IL-1><IL-6><IL1><IL6 Protein><Immune response><Immunological response><Inflammatory><Inflammatory Response><Innate Immune Response><Interleukin I><Interleukin-1><Interleukin-6><Investigation><Lung><Lung Respiratory System><Lung infections><Lymphocyte-Stimulating Hormone><M tb><M tuberculosis><M. tb><M. tuberculosis><MGI-2><Macrophage Cell Factor><Mice><Mice Mammals><Molecular><Murine><Mus><Mycobacterium tuberculosis><Myeloid Differentiation-Inducing Protein><Pathogenesis><Patients><Physiopathology><Plasmacytoma Growth Factor><Pneumonia><Research><SARS Virus><SARS corona virus><SARS corona virus 2><SARS coronavirus><SARS-Associated Coronavirus><SARS-CO-V2><SARS-COVID-2><SARS-CoV><SARS-CoV-1><SARS-CoV-2><SARS-CoV-2 infection><SARS-CoV2><SARS-CoV2 infection><SARS-Related Coronavirus><SARS-associated corona virus 2><SARS-associated coronavirus 2><SARS-coronavirus-2><SARS-related corona virus 2><SARS-related coronavirus 2><SARSCoV2><Severe Acute Respiratory Coronavirus><Severe Acute Respiratory Coronavirus 2><Severe Acute Respiratory Distress Syndrome CoV 2><Severe Acute Respiratory Distress Syndrome Corona Virus 2><Severe Acute Respiratory Distress Syndrome Coronavirus 2><Severe Acute Respiratory Syndrome CoV 2><Severe Acute Respiratory Syndrome Virus><Severe Acute Respiratory Syndrome corona virus><Severe Acute Respiratory Syndrome coronavirus><Severe Acute Respiratory Syndrome-associated coronavirus 2><Severe Acute Respiratory Syndrome-related coronavirus 2><Severe acute respiratory syndrome associated corona virus 2><Severe acute respiratory syndrome coronavirus 2><Severe acute respiratory syndrome coronavirus 2 infection><Severe acute respiratory syndrome related corona virus 2><Shock Lung><Stiff lung><T Helper Factor><Tissues><Viral><Viral Diseases><Virus Diseases><Virus Replication><Work><Wuhan coronavirus><adaptive immune response><adaptive immunity><anti-viral immunity><antiviral immunity><biosafety level 3 facility><causation><co-infection><coinfection><coronavirus disease 2019 infection><coronavirus disease 2019 virus><coronavirus disease-19 virus><cytokine><cytokine release syndrome><cytokine storm><disease causation><hCoV19><host response><immune system response><immunoresponse><in vivo><infected with COVID-19><infected with COVID19><infected with SARS-CoV-2><infected with SARS-CoV2><infected with coronavirus disease 2019><infected with severe acute respiratory syndrome coronavirus 2><innate immune mechanisms><insight><interferon beta 2><life-threatening COVID><life-threatening COVID-19><life-threatening SARS-CoV-2><life-threatening coronavirus disease><life-threatening coronavirus disease 2019><life-threatening severe acute respiratory syndrome coronavirus 2><lung pathogen><lymphocyte activating factor><model of animal><mtb><nCoV2><new therapeutic approach><new therapeutic intervention><new therapeutic strategies><new therapy approaches><new treatment approach><new treatment strategy><novel therapeutic approach><novel therapeutic intervention><novel therapeutic strategies><novel therapy approach><operation><operations><pathogen><pathophysiology><programs><pulmonary><pulmonary infections><pulmonary pathogen><response><serious COVID><serious COVID-19><serious SARS-CoV-2><serious coronavirus disease><serious coronavirus disease 2019><serious severe acute respiratory syndrome coronavirus 2><severe COVID><severe COVID-19><severe COVID19><severe SARS-CoV-2><severe acute respiratory syndrome-CoV><severe coronavirus disease><severe coronavirus disease 19><severe coronavirus disease 2019><severe severe acute respiratory syndrome coronavirus 2><viral infection><viral multiplication><viral replication><virus infection><virus multiplication><virus-induced disease><wet lung>