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|Title:||Elucidating mechanisms of viral hosting in bat reservoirs for emerging zoonotic disease|
|Advisors:||Dobson, Andrew P|
|Contributors:||Ecology and Evolutionary Biology Department|
|Publisher:||Princeton, NJ : Princeton University|
|Abstract:||Bats are the acknowledged reservoir hosts for several of the world’s most virulent emerging zoonotic diseases, including Hendra and Nipah henipaviruses, SARS and MERS coronaviruses, and Ebola and Marburg filoviruses. Bats appear to host these viruses—which are highly pathogenic in other mammals—while experiencing little to no ostensible morbidity or mortality, a phenomenon that has led researchers to question, increasingly, are bats somehow ‘special’ in their capacity as pathogen hosts? Reviews of the literature indicate that bats, which comprise the second-most speciose mammalian order (Chiroptera) and make up ~20% of all mammalian diversity, host a disproportionate number of zoonotic viruses (those viruses which transmit from wildlife to human hosts) as compared with all other mammals. This thesis explores the mechanisms by which bats host virulent infections, at both within-host and cross-population levels. In Chapter One, I delve deeply into the molecular biological underpinnings of bat metabolism, as relates to the evolution of flight, the one characteristic, which—above all—distinguishes Chiropterans from other mammals; I offer insights as to how such evolution might have shaped bat tolerance for, specifically, intracellular (often viral) infections. In Chapter Two, I explore the population-level dynamics of transmission for an intracellular bacterial infection in a community of sympatric Madagascar fruit bats, highlighting the critical reliance of these pathogens on species-specific host-parasite-vector relationships. In Chapter Three, I model the age-structured dynamics of transmission of henipaviruses and filoviruses infecting these same Madagascar fruit bats; I uncover a signature of elevated mortality in seropositive bats, a noteworthy indication of “disease” in these seemingly “special” viral hosts. In Chapter Four, I return once more to the molecular scale to model the dynamics of within-host viral transmission, using data describing the spread of viral infection across monolayers of bat cells. I highlight the critical reliance of bat cells on perpetually primed innate immune responses—a unique feature in mammalian immunity—to contain and control viral pathogenesis. Bats are indeed special, it seems, in their capacity as viral hosts.|
|Alternate format:||The Mudd Manuscript Library retains one bound copy of each dissertation. Search for these copies in the library's main catalog: catalog.princeton.edu|
|Type of Material:||Academic dissertations (Ph.D.)|
|Appears in Collections:||Ecology and Evolutionary Biology|
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