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Jacquelyn Turcinovic Successfully Defends

Congratulations to Jacquelyn Turcinovic on the successful defense of their thesis.

"Methods and Tools for Characterizing Microbial Communities in the Context of Chronic Diseases" Great job Jackie!

To learn more about Jackie's thesis, read their abstract below:


This dissertation is a tale of two emerging human pathogens. The first is a genus of viruses, ebolaviruses, which periodically cause outbreaks in humans in central and western Africa following spillover from animal reservoirs. Ebolavirus outbreaks have high rates of morbidity and mortality and can cause symptoms ranging from vomiting and diarrhea to hemorrhage. Understanding both how the virus evolves to fit its host as well as how the host reacts to viral infection is paramount to understanding what determines whether an infected patient will die or survive ebolavirus infection.


To understand how ebolavirus genomic plasticity allows the virus to optimize itself to its host, I analyzed viral genomic sequencing data from 2 ebolavirus species during serial passage in tissue culture: Ebola virus and Sudan virus. In low-passage Sudan virus, I discovered a true viral quasispecies in which 3-4 viral genotypes circulated within the same stock. I then examined how that quasispecies reacted when put into a nonhuman primate model of infection; unexpectedly we saw that the mix of genotypes that went in matched the mix of genotypes that came out.


To begin to understand what a successful immune response to ebolavirus infection entails, I characterized the circulating transcriptomic response in 2 survival models of Ebola virus disease. In a uniform survival model where nonhuman primates (NHPs) were challenged with Bombali virus, I showed that the animals have a clear and robust response to infection despite varying symptom severity. In a Taï Forest virus challenge model with ~44% survival, I showed that NHPs that succumb do so in a uniform manner consistent with other model of Ebola virus disease. In contrast, survivors were highly variable in their response to infection: some mimicked the non-survivor response but recovered in time, while others hardly responded at all.


After covering ebolavirus genomic plasticity and the host response to ebolavirus infection in the first and second sections, respectively, I will then shift to the other focus of my dissertation work: SARS-CoV-2 and molecular epidemiology. This coronavirus swept the globe in 2020 following spillover into humans from an animal reservoir in late 2019, and surveillance sequencing of viral genomes early in the pandemic showed it was rapidly adapting to its new host. I leveraged this high mutation rate to spin up a molecular epidemiology operation for Boston Medical Center (BMC) and Boston University (BU). From mid-2020 through spring 2022, I catalogued, processed, sequenced, and analyzed samples and viral genomes from over 7000 SARS-CoV-2 patient swabs. I worked with contact tracing teams, physicians, and infection control from BU and BMC to quantify viral introductions, identify transmission chains, and integrate the genetic linkages with traditional epidemiological data.

Major Professor: John Connor


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