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    Influenza A Virus Induced Programmed Cell Death

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    Genre
    Thesis/Dissertation
    Date
    2020
    Author
    Shubina, Maria
    Advisor
    Balachandran, Siddharth
    Committee member
    Monestier, Marc
    Rall, Glenn F.
    Tempera, Italo
    Kilpatrick, Laurie
    Carey, Alison J.
    Department
    Cancer Biology & Genetics
    Subject
    Cellular Biology
    Apoptosis
    Cell Death
    Influenza
    Necroptosis
    Ripk3
    Small Molecules
    Permanent link to this record
    http://hdl.handle.net/20.500.12613/3565
    
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    DOI
    http://dx.doi.org/10.34944/dspace/3547
    Abstract
    Influenza A viruses (IAV) are negative sense RNA viruses that naturally infect a wide variety of animals. Different subtypes of the virus infect waterfowl, poultry, pigs, horses, ferrets, bats, dogs, cats and humans, causing zoonotic outbreaks and pandemics. In humans, IAV strains cause seasonal epidemics that can result in up to 50000 deaths and 700000 hospitalizations each year, and ranks in the top ten causes of death in the United States. In addition, virulent strains of IAV have caused pandemic outbreaks triggering numerous fatalities. While tropism to the upper respiratory tract is important for virus transmission, infection of the lower lung is most correlated with pathogenesis. The mammalian lung has multiple structural cell types, of which two classes are considered most important for IAV pathogenesis. These are (1) alveolar unit cells and (2) cells of the conducting airways, primarily those of the bronchi and bronchioles. Alveolar unit cells, or pneumocytes, chiefly comprise type I and type II alveolar epithelial cells, and are involved in gas exchange and surfactant production. Cells of the bronchi and bronchioles (e.g., basal, secretory, ciliated, club, goblet and neuroendocrine cells) perform numerous functions related to tissue repair/renewal, and mucous production. Upon IAV infection the regulated (or programmed) death of the infected cell represents an important pathogen clearance mechanism. Programmed cell death can be largely non-inflammatory (e.g., apoptosis) or pro-inflammatory (e.g., necroptosis). In this dissertation, I outline experiments carried out to identify the role of pro-inflammatory programmed cell death in influenza A virus clearance and pathogenesis both in vitro and in vivo. My work outlines the role of necroptosis in IAV clearance, and how this controlled form of cell death, particularly in alveolar unit cells, can be exploited as a potential new therapeutic avenue for severe influenza disease.
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